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THE PEPTIC ULCER DISEASE IN BORAMA

BY MOHAMOUD MOHAMED MOHAMOUD REG.NO=1720

A research report is submitted in partial fulfillment requirement for assignment of research methodology of medicine and surgery of Amoud University

Prof. Abib adan

Borama Somaliland

May 2012

Acknowledgements
Firstly,It is almightily praise to Allah, the creator of the world. Second I would like to thank all of my friends who encouraged me to make this research and all of them who helped and made me possible to carry out this task.

Research contents 1: Introduction to peptic ulcer disease 2: peptic ulcer disease in borama 3: the causes of peptic ulcer disease 4: effects to population in borama

Introduction to peptic ulcer disease in borama.

Burning epigastric pain exacerbated by fasting and improved with meals is a symptom complex associated with peptic ulcer disease (PUD). An ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation. Ulcers occur within the stomach and/or duodenum and are often chronic in nature. Acid peptic disorders are very common in this region, with 80 0/0 individuals (new cases and recurrences) affected per year.

PUD occurs most commonly in duodenal bulb (duodenal ulcerDU) and stomach (gastric ulcerGU). It may also occur in esophagus, pyloric channel, duodenal loop, jejunum, Meckels diverticulum. PUD results when aggressive factors (gastric acid, pepsin) overwhelm defensive factors involved in mucosal resistance (gastric mucus, bicarbonate, microcirculation, prostaglandins, mucosal barrier), and from effects of Helicobacter pylori. Peptic ulcer disease is one of the common diseases in this community, and it became the most widespread disease that is diagnosed by many people every day. Although it is not recorded well the cases that encountered in the hospital, I tried to make some research that helps me feel the problem which faces our community when I was doing my normal duty and my education in the hospital. In fact it is difficult to get the correct information about this problem,

because there is no record that I can get the former information such cases before years or decades so the classification of the increasing and decreasing of the disease is very difficult. But in my trail research, it seems that this disease increases fast as compared to other chronic diseases. This disease has major effect in this community ( especially the people who live low life but not always true).Although this is the normal disease of this community geographically, it may exist the other community outside this community. There are many things that induced me to know this problem such the increasing the number of people who died the outcomes or the consequences from it, the increasing number of the people who are suffering from it and complaining its troublesome effects. Epidemiologically this disease varies throughout the world and depends largely on the overall standard of living in the region. In developing parts of the world, 80% of the population may be infected by the age of 20, whereas the prevalence is 2050% in industrialized countries. In contrast, in the United States this organism is rare in childhood.

peptic ulcer disease in borama

There are many people who have suffered from peptic ulcer disease and it became the most common chronic disease in this community. Although it cannot be revealed the accurate information of this disease by laboratories due to their fault, There are more than five laboratories which I have taken the following data. The first data is taken from borama general laboratory and its clinical diagnosis indicates that 20 0/0 outpatient had peptic ulcer disease while 5 0/0 had its chronic effects and the other laboratories indicates same as this one. Some report, which was written by some medical student, I found in the emergency office of the borama general hospital ,this report was collected the inpatient who was suffered by peptic ulcer disease and indicated that majority of the inpatients had diagnosed peptic ulcer disease.the patients report can found in the hospital though most of the report are not collected well and when the patient is either discharged or died, is discarded. Last month, one of the senior medical students in Amoud University took questionnaires about peptic ulcer disease. This questionnaire consisted of five pages and the site is dareymaane community sector. The people, who were questioned, are the resident of dareymaane. This questionnaire gave us data that indicates the incidence of the disease that we can take account for it. The age of the people who was questioned is about 50-68 years out of 20 persons. So that this disease affect the majority of the in all ages even the young adults of this town. There is another interesting information which reveals that this disease is endemic to this town because the student who came from other regions told me that when they came here they suffered from PUD and when they come back to their regions they felt healthy, so in case of this there is some etiologic factors which need scientific investigation to the fact of the causative things.

In my view point, I believe that there are many things which causes this disease in this town, either can be life style such as food, water and importing materials such as oil or psychological problems like stress which is the major contributor of this disease. So I am informing the researchers to do this condition which is getting worse day after day.

The causes of peptic ulcer disease

Major role for H. pylori, spiral urease-producing organism that colonizes gastric antral mucosa in up to 100% of persons with DU and 80% with GU. Also found in normals (increasing prevalence with age) and those of low socioeconomic status. Invariably associated with histologic evidence of active chronic gastritis, which over years can lead to atrophic gastritis and gastric cancer. Other major cause of ulcers is NSAIDs (those not due to H. pylori). Fewer than 1% are due to gastronome (Zollinger-Ellison syndrome). Other risk factors and associations: hereditary (? increased parietal cell number), smoking, hypercalcemia, mastocytosis, blood group O (antigens may bind H. pylori). Unproven: stress, coffee, alcohol. DU Mild gastric acid hypersecretion resulting from (1) increased release of gastrin, presumably due to (a) stimulation of antral G cells by cytokines released by inflammatory cells and (b) diminished production of somatostatin by D cells, both resulting from H. pylori infection; and (2) an exaggerated acid response to gastrin due to an increased parietal cell mass resulting from gastrin stimulation. These abnormalities reverse rapidly with eradication of H. pylori. However, a mildly elevated maximum gastric acid output in response to exogenous gastrin persists in some pts long after eradication of H. pylori, suggesting that gastric acid hypersecretion may be, in part, genetically determined. H. pylori may also result in elevated serum pepsinogen levels. Mucosal defense in duodenum is compromised by toxic effects of H. pylori infection on patches of gastric metaplasia that result from gastric acid hypersecretion or rapid gastric emptying. Other riskfactors include glucocorticoids, NSAIDs, chronic renal failure, renal transplantation, cirrhosis, chronic lung disease. GU H. pylori is also principal cause. Gastric acid secretory rates usually or reduced, possibly reflecting earlier age of infection by H. pylori than in DU pts. Gastritis due to reflux of duodenal contents (including bile) may play a role. Chronic salicylate or NSAID use may account for 1530% of GUs and increase riskof associated bleeding, perforation. CLINICAL FEATURES DU Burning epigastric pain 90 min to 3 h after meals, often nocturnal, relieved by food. GU Burning epigastric pain made worse by or unrelated to food; anorexia, food aversion, weight loss (in 40%). Great individual variation. Similar symptoms may occur in persons without demonstrated peptic ulcers (nonulcer dyspepsia); less responsive to standard therapy. COMPLICATIONS Bleeding, obstruction, penetration causing acute pancreatitis, perforation, intractability.

TREATMENT
Objectives: pain relief, healing, prevention of complications, prevention of recurrences. For GU, exclude malignancy (follow endoscopically to healing). Dietary restriction unnecessary with contemporary drugs; discontinue NSAIDs; smoking may prevent healing and should be stopped. Eradication of H. pylori markedly reduces rate of ulcer relapse and is indicated for all DUs and GUs associated with H. pylori (Table 150-2). Acid suppression is generally included in regimen. Standard drugs (H2-receptor blockers, sucralfate, antacids) heal 8090% of DUs and 60% of GUs in 6 weeks; healing is more rapid with omeprazole (20 mg/d). Surgery For complications (persistent or recurrent bleeding, obstruction, perforation) or, uncommonly, intractability (first screen for surreptitious NSAID use and gastrinoma).

TRIPLE THERAPY
1. Bismuth subsalicylate plus Metronidazole plus Tetracyclinea 2. Ranitidine bismuth citrate plus Tetracycline plus Clarithromycin or metronidazole 3. Omeprazole (lansoprazole) plus Clarithromycin plus Metronidazoleb or Amoxicillinc 1 g bid 2 tablets qid 250 mg qid 500 mg qid 400 mg bid 500 mg bid 500 mg bid 20 mg bid (30 mg bid) 250 or 500 mg bid 500 mg bid

dose

QUADRUPLE THERAPY
Omeprazole (lansoprazole) Bismuth subsalicylate Metronidazole Tetracycline 20 mg (30 mg) daily 2 tablets qid 250 mg qid 500 mg qid