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Peptic ulcers occur in the part of gastrointestinal tract which is exposed to gastric acid and pepsin. A peptic ulcer of the stomach is called a gastric ulcer; of the duodenum, a duodenal ulcer; and of the esophagus, an esophageal ulcer. It most commonly occurs in gastric antrum or duodenal bulb as showed in figure 1.  An ulcer develops when the lining of this organ is corroded by the acidic digestive juices which are secreted by the stomach cells which are also known as parietal cells. These digestive juices consist of pepsin, rennin, hydrochloric acid and mucus.  Lesions more than 5 mm are called ulcers, whereas those smaller than 5 mm are called erosions.  The mucous membrane lining the digestive tract erodes and causes gradual breakdown of tissue. This breakdown causes burning pain in the upper middle part of the abdomen.  Although most peptic ulcers are small, it can cause a considerable amount of discomfort. Peptic ulcer disease is a worldwide problem and the lifetime risk of acquiring the disease is approximately 1 in 10. 
Figure 1: The site of peptic ulcers. 
The development of peptic ulcer is not entirely understood. It results probably due to an imbalance between the aggressive acid, pepsin, and Helicobacter pylori and the defensive gastric mucous, bicarbonate secretion, prostaglandins, and nitric oxide. In gastric ulcer, generally acid secretion is normal or low, whereas duodenal ulcers are generally characterized by increased level of acid secretion. Both can occur in the setting of Helicobacter pylori infection. 
Common Causes of Peptic Ulcers :
For many years excess gastric acid secretion was believed to be the major cause of the ulcer. While acid is still considered significant in ulcer formation, the leading cause of peptic ulcer is currently believed to be infection of the stomach by bacteria called Helicobacter pylori (H.pylori). Initially it was known as Campylobacter pyloridis when it was first found on 1984. Helicobacter pylori is a spiral shaped, gram-negative bacteria and it is unique in its ability to survive within the hostile acid environment of the stomach. Its shape and flagella allow penetration and passage through the gastric mucous layer while its urease activity appears essential for colonization and survival. It lives within the gastric mucous layer, somewhat protected from stomach acid. It has a potent urease activity, which hydrolyzes urea to ammonia and bicarbonate and increases its resistance to the stomach's low pH environment. Helicobacter pylori is able to adhere tightly to the epithelial cell surface and it generally does not directly invade the epithelial cells but indirectly makes the gastric mucosa more vulnerable to acid peptic damage by disrupting the mucous layer, liberating a variety of toxins. In addition, the host immune response to Helicobacter pylori incites inflammatory reactions that further bring about tissue injury. This chronic inflammation upsets gastric acid secretory physiology to varying degrees and leads to chronic gastritis, which in most individuals, is asymptomatic but, in some will lead to ulcers and even gastric cancer. 
Another major cause of the peptic ulcers is the chronic use of anti-inflammatory drugs, commonly referred as nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. Prostaglandins are substances which are important in helping the gut linings resist corrosive acid damage. NSAIDs cause ulcers by interfering with prostaglandins in the stomach.
The risk of peptic ulcer and gastrointestinal bleeding are dependent on the dose, duration, and type of NSAID.  NSAID has a direct toxic effect because of its acidic nature and it can decrease the hydrophobicity of gastric mucous, allowing injury of the epithelium by gastric acids. 
Cigarette smoking also promotes the development of peptic ulcers and may interact with Helicobacter pylori and NSAIDs to increase mucosal injury. Smoking also impairs ulcer healing and increases ulcer recurrence. Alcohol, caffeine, spicy foods have no proven evidence in ulcer formation. 
Signs and Symptoms:
Epigastric pain is the classic symptom associated with peptic ulcer disease. The pain is often described as gnawing, dull, aching, "empty", "hunger-like" sensation. In contrast, some patients will experience pain after eating. During fasting they may have relief of their symptoms, which then recur shortly after eating. As a result, some patients experience nausea, avoidance of food, and even weight loss. However, many patients present with few or no symptoms until the development of complications such as gastrointestinal bleeding, perforation, penetration and obstruction.
Diagnosis of peptic ulcer:
Definitive diagnosis of peptic ulcers can be made with upper endoscopy. Patient suspected of having an ulcer who present with alarm symptoms such as gastrointestinal bleeding, unexplained weight loss, and those who are elderly will undergo prompt evaluation with endoscopy. Several types of test have been developed to detect the presence of Helicobacter pylori. This test includes serology (tests for IgG antibodies to Helicobacter pylori), and urease assays (tests for presence of the urease enzyme, which is produced in high amounts by Helicobacter pylori). 
Medications used to treat peptic ulcers include H2-receptor blockers (ranitidine, cimetidine, and famotidine), proton pump inhibitors (esomeprazole, lansoprazole, and omeprazole). Both types of drug reduce gastric acid secretion in stomach.
Appropriate therapy should be given for eradication of Helicobacter pylori. The success of it depends on the type and duration of therapy, patient compliance and bacterial factors such as antibiotics resistance. Some commonly used antibiotics are amoxicillin and clarithromycin.
Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are the major causes of peptic ulcer. Only some may develop the sign and symptoms of this disease. Patient who are suspected having peptic ulcer have to undergone the diagnosis tests and medications such as H2-receptor blockers and proton pump inhibitor are the most commonly prescribed.