Peptic ulcer Disease

In common terms Ulcer means an open sore and word peptic is related to acid so Peptic ulcer means an open sore due to acid in Gastrointestinal tract.

In medical terms Peptic ulcer is an open sore which develops in the lining of gastro-intestinal tract that causes pain in stomach.

Peptic ulcers are of two types

1. Gastric ulcer – which is located in the inner lining of the stomach.
2. Duodenal ulcer – which is located in the duodenum or beginning of small intestine.

Both ulcers penetrate the muscularis mucosa but erosions do not penetrate the muscularis mucosa.
Peptic ulcer may be acute or chronic.

Pathophysiology

Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.
In normal condition a physiologic balance exists between production of acid or diffusion of hydrogen ion and bicarbonates and production of protective mucus, when the balance between the aggressive factors (acid secretion) and the defensive mechanisms is disrupted, results in mucosal injury.

Aggressive factors

1. H. Pylori
Peptic ulceration is strongly associated with H. pylori (Helicobacter Pylori) infection.
These infections are probably acquired in childhood by person-to-person contact. The vast majority of colonized people remain healthy and asymptomatic and only a minority develops clinical disease.
H. pylori is Gram-negative and spiral, and has multiple flagella at one end, which make it motile, allowing it to burrow and live beneath the mucus layer adherent to the epithelial surface. H. pylori exclusively colonizes gastric-type epithelium and is only found in the duodenum in association with patches of gastric metaplasia. It causes chronic gastritis by provoking a local inflammatory response in the underlying epithelium.
In most people, H. pylori causes localized antral gastritis associated with depletion of somatostatin (from D cells) and increased gastrin release from G cells. Virulence factors produced by H pylori, including urease, catalase, vacuolating cytotoxin, and lipopolysaccharide, are well described.
The ulcer probably arises because of impaired mucosal defense resulting from a combination of H. pylori infection, NSAIDs and smoking, rather than excess acid.
2. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
Treatment with NSAIDs is associated with peptic ulcers. These are a group of pain-killer drugs which are most easily available drugs without prescriptions. Over uses of non-selective NSAIDs can damage the gastric and duodenal mucosal barrier and are associated with an increased risk of upper gastrointestinal ulceration, bleeding and perforation.
3. Smoking
Smoking and tobacco use is also associated with risk of developing duodenal and gastric ulcers. Once the ulcer has formed, it is more likely to cause complications and less likely to heal if the patient continues to smoke.
4. Alcohol intake
Drinking alcohol is also associated with gastric and duodenal ulcers. Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis.
5. Severe physiologic stress
Stressful conditions that may cause PUD include burns, CNS trauma, surgery, and severe medical illness. Serious systemic illness, sepsis, hypotension, respiratory failure, and multiple traumatic injuries increase the risk for secondary (stress) ulceration.
Local radiation resulting in mucosal damage, which may lead to the development of duodenal ulcers
6. Sleep deprivation, sedentary lifestyle, eating habits, anxiety and depression are also common factors associated with peptic ulcer.

Signs and Symptoms

The most common symptom is recurrent abdominal pain which may be dull or sharp which has three important characteristics; localization to the epigastrium, relationship to food and episodic occurrence. Sometimes food makes the pain better, and sometimes it makes it worse. Other symptoms include nausea, vomiting, or feeling bloated or full. It is important to know that there are many causes of abdominal pain, so not all pain in the abdomen is an “ulcer”.
Sometimes in elderly people or the people taking NSAIDS for the years have no symptoms or very vague abdominal pain, these are silent ulcers and usually diagnosed first time when they develop anemia from undetected chronic blood loss.
Occasionally, the only symptoms are anorexia and nausea, or early satiety after meals.

Investigations

To know the cause of pain in abdomen your doctor may order the following tests
Testing for H pylori infection is essential in all patients with peptic ulcers.

1. Bood test – CBC count and Iron studies are useful to detect anemia. Anemia is an alarm signal for peptic ulcer disease and further investigations with endoscopy to rule out other disorders.
2. Liver function test, amylase and lipase may also be useful depending upon signs and symptoms.
3. Urea breath test – Urea breath tests detect active H pylori infection by testing for the enzymatic activity of bacterial urease. For a urea breath test, you will drink a special liquid that contains urea, a waste product that your body makes as it breaks down protein. If H. pylori are present, the bacteria will change this waste product into carbon dioxide and ammonia—a harmless gas. Carbon dioxide normally appears in your breath when you exhale.
In the presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope, carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.
This test has high sensitivity and specificity but it needs expensive mass spectrometer.
4. Stool test – In the presence of H.pylori bacteria antigens can be seen on stool, also called as fecal antigen test. Fecal antigen testing identifies active H pylori infection by detecting the presence of H pylori antigens in stools. This test is more accurate than antibody testing and is less expensive than urea breath tests.
5. Endoscopy – Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected PUD. It is highly sensitive for the diagnosis of gastric and duodenal ulcers, allows for biopsies and cytologic brushings in the setting of a gastric ulcer to differentiate a benign ulcer from a malignant lesion, and allows for the detection of H pylori infection with antral biopsies for a rapid urease test and/or histopathology in patients with PUD.
An upper GI endoscopy is performed by inserting a special lighted camera on a flexible tube into the person’s mouth to look directly into the stomach and the beginning of the small bowel. This flexible camera carefully inspects the most likely areas for ulcers to be located.

Treatment

The aims of management are to relieve symptoms, induce healing and prevent recurrence. H. pylori eradication is the cornerstone of therapy for peptic ulcers, as this will successfully prevent relapse and eliminate the need for long-term therapy in the majority of patients.

H. pylori eradication
The recommended primary therapy for H pylori infection is proton pump inhibitor (PPI)–based triple therapy. PPI and two antibiotics (from amoxicilline, clarithromycine and metronidazole) for 7 -14 days but high dose twice daily for longer duration (14days) is more effective, Amoxicillin should be replaced with metronidazole in penicillin-allergic patients only, because of the high rate of metronidazole resistance.
(PPI + Clarithromycine + Amoxicilline) PO twice daily for 14 days.
Or
(PPI + Clarithromycine +Metronidazole) PO twice daily for 14 days.
Quadruple therapy
Quadruple therapies for H pylori infection are generally reserved for patients in whom the standard course of treatment has failed. a quadruple therapy regimen, consisting of omeprazole (or another PPI), bismuth subcitrate, metronidazole and tetracycline (OBMT) for 10–14 days.
For those who are still colonised after two treatments, the choice lies between a third attempt guided by antimicrobial sensitivity testing, rescue therapy (levofloxacin, PPI and clarithromycin) or long-term acid suppression.

Maintenance treatment
Continuous maintenance treatment should not be necessary after successful H. pylori eradication. For the minority who do require it, the lowest effective dose of PPI should be used.

Surgical treatment
Surgery is now rarely required for peptic ulcer disease but it is needed in some cases.

General preventive measures

1. Unnecessary use of NSAIDS should be avoided.
2. Smoking is always dangerous for health, should be avoided.
3. Use of aspirin should be avoided.
4. Use acetaminophen or nonacetylated salicylates when possible.
5. Alcohol use should be avoided.
6. Follow healthy lifestyle.

Please note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional.
Content source – Davidson’s Principles and Practice of Medicine(22ndedition)
http://patients.gi.org/topics/peptic-ulcer-disease/
http://emedicine.medscape.com/article

Advertisements