The male to female ratio for duodenal ulcer varies from 5:1 to 2:1, for gastric ulcer is 2:1 or less

The prevalence of duodenal ulcer is estimated to be 6-15% in the general population. The prevalence is linked to the presence of H pylori. Overall, the incidence of duodenal ulcer has been decreasing over the past 3-4 decades.

o Causes

Table 1. Causes of Gastroduodenal Ulcers
Cause	Comments
Common
Helicobacter pylori infection	Gram-negative, motile spiral rod found in 48 % of patients with PUD
NSAIDs	5 to 20 % of patients who use NSAIDs over long periods develop PUD NSAID-induced ulcers and complications are more common in older patients, patients with a history of ulcer or gastrointestinal bleeding, those who use steroids or anticoagulants, and those with major organ impairment
Other medications	Steroids, bisphosphonates, potassium chloride, chemotherapeutic agents (e.g., intravenous fluorouracil)
Rare
Acid-hypersecretory states (e.g., Zollinger-Ellison syndrome)	Multiple gastroduodenal, jejunal, or esophageal ulcers
Malignancy	Gastric cancer, lymphomas, lung cancers
Stress	After acute illness, multiorgan failure, ventilator support, extensive burns (Curling's ulcer), or head injury (Cushing's ulcer)

• H pylori - In the industrialised world the prevalence of H. pylori infection in the general population rises steadily with age, and in the UK approximately 50% of those over the age of 50 years are infected. In many parts of the underdeveloped world infection is much more common and is often acquired in childhood.

§ Gastrinoma (Zollinger-Ellison syndrome [ZES]) caused by a tumor of pancreatic islet cells that produces gastrin. It is associated with gastric acid hypersecretion and development of PUD. From 0.1-1% of duodenal ulcers are thought to be secondary to an underlying gastrin-secreting tumor.

§ Crack cocaine: Use of crack cocaine causes localized vasoconstriction, and the reduced blood flow may lead to mucosal damage.

The vast majority of colonised people remain healthy and asymptomatic and only a minority develop clinical disease

Pathogenesis and pathophysiology of infection.

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. A portion of the gastric and duodenal mucus 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.

H. pylori motility allows it to localise and live deep beneath the mucus layer closely adherent to the epithelial surface. Here the surface pH is close to neutral and any acidity is buffered by the organism's production of the enzyme urease. This produces ammonia from urea and raises the pH around the bacterium. Although it is non-invasive, the bacterium stimulates chronic gastritis by provoking a local inflammatory response in the underlying epithelium due to release of a range of cytotoxins. H. pylori exclusively colonises gastric-type epithelium and is only found in the duodenum in association with patches of gastric metaplasia.

In most people H. pylori causes antral gastritis associated with depletion of somatostatin (from D cells) and gastrin release from G cells. The subsequent hypergastrinaemia stimulates acid production by parietal cells, but in the majority of cases this has no clinical consequences. In a minority of patients this effect leads to duodenal ulceration. The role of H. pylori in the pathogenesis of gastric ulcer is less clear but H. pylori probably reduces gastric mucosal resistance to attack from acid and pepsin. In 1% of infected people, H. pylori causes a pangastritis leading to gastric atrophy and hypochlorhydria. This allows bacteria to proliferate within the stomach; these may produce mutagenic nitrites from dietary nitrates, predisposing to the development of gastric cancer.

Ulcers occur only in the presence of acid and pepsin; they are never found in achlorhydric patients such as those with pernicious anaemia.

PUD a chronic condition with a natural history of spontaneous relapse and remission lasting for decades, if not for life. Although they are different diseases, duodenal and gastric ulcers share common symptoms which will be considered together.

The main symptoms of PUD:

- Recurrent Abdominal pain:

- localization (epigastrium) and radiation,

- character (episodic occurrence), permanent or seasonal

- relationship to food (early, late, nocturnal, hunger).

- Dyspepsia: (vomiting, nausea, heartburn)

- Relieving factors (taking food or soda, spasmolytics, warmly)

- Possible clinical features (weight loss, fever, anorexia, dysphagia).

Clinical symptoms of PUD:

- Tender palpation of the abdomen: local pain (tenderness)

- Local muscular resistance

- Mendel’s symptom in epigastrium or duodenum bulb projection point in percussion

Auscultation of the abdomen: gastric’s down border,

• If the initial clinical presentation suggests the diagnosis of PUD, the patient should be evaluated for alarm symptoms.

Anemia, hematemesis, melena, or heme-positive stool suggests bleeding; vomiting suggests obstruction; anorexia or weight loss suggests cancer; persisting upper abdominal pain radiating to the back suggests penetration; and severe, spreading upper abdominal pain suggests perforation. Patients older than 55 years and those with alarm symptoms should be referred for prompt upper endoscopy.

Additional investigations.

- analyze the barium meal examination

- upper GI endoscopies

- evidence of H. pylori infection

- pH data

Дата добавления: 2015-07-25