Peptic ulcer disease

DEFINITION,HSTORY,ETIOLOGY,EPIDEMIOLOGY,PATHOGENESIS,PHARMACOLOGICAL & NON -PHARMACOLOGICAL TREATMENT OF PEPTIC ULCER DISEASE.

1. PEPTIC ULCER DISEASE BY HEENA PARVEEN

2. PEPTIC ULCER DISEASE The term ‘peptic ulcer’ describes a condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa that persists as a result of acid and pepsin in the gastric juice.

3. HISTORY Helicobacter pylori  was identified in 1982 by two Australian scientists,  Robin Warren and Barry J. Marshall, as a causative factor for ulcers . Barry J. Marshall Robin Warren

4. ETIOLOGY Upper abdominal pain. Anorexia , Weight loss, N ausea and vomiting , Heartburn Eructation/BURPING/BELCHING Patients with predominant symptoms of heartburn are likely to have GORD. Haemorrhage , Chronic iron-deficiency anaemia , Pyloric stenosis and perforation .

5. EPIDEMIOLOGY About 10% of the population in developed countries is likely to be affected at some time by peptic ulcer, with the prevalence for active ulcer disease being about 1% at any particular point in time. Infection by H. pylori, a spiral bacterium of the stomach, remains an important epidemiological factor in causing peptic ulcer. The most important risk factors for H. pylori infection are low social class, overcrowding and home environment during childhood, for example, bed sharing. There may be other genetic, environmental or cultural factors influencing peptic ulcer disease .

6. Helicobacter pylori. The Gram-negative spiral bacterium H. pylori, formerly known as Campylobacter pylori, was isolated serendipitously from patients with gastritis by Barry Marshall and Robin Warren in 1982. Seven years later, it was conceded that H. pylori is responsible for most cases of gastric and duodenal ulcer.

7. Pathogenesis There are 2 common forms of peptic ulcer disease: with the organism H. pylori & with the use of aspirin and NSAIDs . Less common is ulcer disease associated with massive hypersecretion of acid which occurs in the rare gastrinoma (Zollinger–Ellison) syndrome. The underlying pathophysiology associated with H. pylori infection involves the production of cytotoxin -associated gene A ( CagA ) proteins and vacuolating cytotoxins , such as vac A, which activate the inflammatory cascade. A number of enzymes produced by H. pylori may be involved in causing tissue damage and include urease , haemolysins , neuraminidase and fucosidase . High acid content in the proximal duodenum leads to metaplastic gastric-type mucosa , which provides a niche for H. pylori infection followed by inflammation and ulcer formation .

8. Three patterns of mucosal damage are caused by NSAIDs. These include superficial erosions and haemorrhages , silent ulcers detected at endoscopy and ulcers. Weak acid NSAIDs, such as acetylsalicylic acid, are concentrated from the acidic gastric juice into mucosal cells,& may produce acute superficial erosions via inhibition of COX and by mediating the adherence of leucocytes to mucosal endothelial cells. Enteric coating may prevent this superficial damage but does not demonstrate any clinical benefit in terms of reduction of gastro-intestinal bleeding or ulceration. The presence of NSAID-induced ulcers does not correlate with abdominal pain and NSAIDs themselves often mask ulcer pain . Smoking leads to Atherosclerosis & vascular spasms– causes vascular insufficiency & promote Ulcer development.

9. Diagnosis

10. Non-Pharmacological treatment

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12. MECHANISM OF ACTION OF DRUGS

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