the peptic ulcer disease in borama

7/29/2019 The Peptic Ulcer Disease in Borama

1/6

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


2/6

Research assignment contents

1: Introduction to peptic ulcer disease

The definition of pud

Types of pud

2: Peptic ulcer disease in borama

The reason of the study

Reports of the inpatient and outpateints

The questionnaire of dareymaane

3: The causes of peptic ulcer disease

4: The treatments of peptic ulcer disease


3/6

1: Introduction to peptic ulcer disease

Burning epigastric pain exacerbated by fasting and improved with meals is a symptom complex

associated with peptic ulcer disease (PUD). An ulceris 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 ofHelicobacter 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 beinfected 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.


4/6

2: 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 fivelaboratories 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.

3: 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

histological 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


5/6

associations: hereditary (? increased parietal cell number), smoking, hypercalcemia,

mastocytosis, blood group O (antigens may bind H. pylori). Unproven: stress, coffee, alcohol.

DUMild 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. pyloriinfection; and

(2) an exaggerated acid response to gastrin due to an increased parietal cell mass resulting fromgastrin stimulation. These abnormalities reverse rapidly with eradication ofH. pylori. However,

a mildly elevated maximum gastric acid output in response to exogenous gastrin persists in

some pts long after eradication ofH. pylori, suggesting that gastric acid hypersecretion may be,

in part, genetically determined. H. pylorimay also result in elevated serum pepsinogen levels.

Mucosal defense in duodenum is compromised by toxic effects ofH. pyloriinfection 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. GUH. pyloriis also principal cause. Gastric acid secretory rates

usually or reduced, possibly reflecting earlier age of infection by H. pylorithan 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

DUBurning epigastric pain 90 min to 3 h after meals, often nocturnal, relieved by food.

GUBurning 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.

TREATMENTObjectives: 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 ofH. pylorimarkedly 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).

SurgeryFor complications (persistent or recurrent bleeding, obstruction, perforation) or, uncommonly,

intractability (first screen for surreptitious NSAID use and gastrinoma).

TRIPLE THERAPY dose1. Bismuth subsalicylateplus 2 tablets qidMetronidazoleplus 250 mg qid


6/6

Tetracyclinea 500 mg qid

2. Ranitidine bismuth citrateplus 400 mg bid

Tetracyclineplus 500 mg bid

Clarithromycin ormetronidazole 500 mg bid

3. Omeprazole (lansoprazole)plus 20 mg bid (30 mg bid)

Clarithromycinplus 250 or 500 mg bidMetronidazoleb or 500 mg bid

Amoxicillinc 1 g bid

QUADRUPLE THERAPYOmeprazole (lansoprazole) 20 mg (30 mg) daily

Bismuth subsalicylate 2 tablets qid

Metronidazole 250 mg qid

Tetracycline 500 mg qid

References include:

Borama general hospital data

Allaale hospital data and other laboratories

The questionnaire of senior medical students in daraymaane

The Harrisons book

The interview.

the peptic ulcer disease in borama

Documents