Disease Profile: Peptic Ulcer Epidemiology - Essay Example

INTRODUCTION There are actually different kinds of ulcers and Peptic Ulcer is practically one of the most common ones. Peptic Ulcer, or also known asUlcus Pepticum, is noted as a practically defined ailment of the stomach that happens in the gastrointestinal tract making the said medical problem extremely painful. The occurrence of Peptic Ulcer could be caused by several elements including use of aspirin and other drugs such as NSAID's. Unlike old time knowledge, doctors recently found out that it is not stress that forces the occurrence of peptic ulcer in the stomach. Apparently, bacterial infections and further stomach upsetting medications causes the occurrence of peptic ulcer. Figure 1: Peptic Ulcer Defined From this figure, it could be seen how a peptic ulcer appears to be a swollen part within the pylorus that affects the passage towards the duodenum making the ailment highly painful when digestion is undergone in the stomach. EPIDEMIOLOGY The word peptic relates to pepsin (or acid); thus, peptic ulcer disease points to gastric and-or duodenal ulcer or erosion (Shashidhar et al, 2009). It has been suggested that a peptic ulcer is a breach in the epithelium that penetrates the muscularis mucosa layer, which if not breached and then it is erosion. Agent: as per noted earlier, it could be considered that the major agent for the existence of peptic ulcer in a person is that of stomach-upsetting medication such as aspirin intake and NSAID's. This could also include bacterial infections that grow within the stomach causing over production of acidic substances in the duodenum towards the small intestines and the stomach itself. Environmental Conditions: peptic ulcers choose no particular environmental setting. Usually though, people who develop this particular ailment are noted for eating too much spicy food, alcoholic beverages and other food sources that could be a great source of acidic development in the stomach. Occupational Risks: people who are working 24/7 at work missing food and missing meals are usually most prone to this particular ailment. Nevertheless, it could be considered that the individuals taking regular aspirin-based medication to regulate certain systems in their body could also be most in danger of developing this ailment. PATHOPHYSIOLOGY Gastric HCl production is stimulated by gastrin secreted by G cells in the antrum, acetylcholine released by the vagus nerve and histamine released by enterochromaffin-like (ECL) cells, all of which stimulate receptors on acid-producing parietal cells. Duodenal ulcers are rare in people who do not produce gastric acid and gastric acid production is usually low in people with gastric ulcers. CLINICAL PRESENTATION/DIAGNOSIS Severity of symptoms relates to the presence of multiple duodenal ulcers, ulcers distal to the duodenal bulb, a strong family history, ulcers that are refractory to medical therapy and ulcers that recur after surgery. Peptic ulcers in subjects who are H pylori-negative and negative for NSAIDs may point to Zollinger-Ellison syndrome. Complications relate to NSAID use or chronic peptic ulcers, the development of ulcer symptoms or a change in symptoms pattern precede the onset of complications. However, complications are the presenting symptom of a peptic ulcer disease in clinically silent cases. Penetrating ulcers usually present with a change of the character of pain from the vague visceral discomfort to a localized and intense pain radiating to the back; besides, the expected relief of food or antacids diminishes. Vomiting is a key feature in cases of pyloric outlet obstruction and bleeding peptic ulcer may be preceded by nausea and is in the form of haematemesis or melena (Soll and Graham, 2008) GIT endoscopy is a key to diagnosis of peptic ulcer disease, complication and for differential diagnosis from other causes of dyspepsia. In addition, endoscopic healing is the gold standard in treatment evaluation. Upper GIT double-contrast radiography may be of equal diagnostic accuracy. However, radiological studies are not as sensitive as endoscopy especially for the diagnosis of small ulcers (less than 0.5 cm). Further, radiological studies do not allow biopsy needed for differential diagnosis, ruling out malignancy or access to H pylori infection diagnosis. The main indication for CT scan is when considering other associated condition and chest x-ray is useful to detect free abdominal air in case perforation is a possibility. Diagnosis of H pylori infection by non-invasive methods as serological tests depends on identification of the organism's specific IgG antibodies. Breath test where the patient drinks C13 or C14 labeled urea, since H pylori rapidly metabolizes urea, C13 or C14 is absorbed and is expired as CO2 and can be used as an indication of infection. Invasive (endoscopy dependent) methods include the biopsy urease test, which depends on the organism's ability to produce urease. Histological identification of the organism and finally, culture of the biopsy specimen is useful for antibiotic susceptibility testing. TREATMENT 7.1 Anti-secretory drugs Histamine H2-receptor antagonists (H2RAs) are competitive reversible inhibitors of histamine binding at H2-receptors on parietal cells. They are effective and safe but differ in potency with cimetidine is the least potent of the H2RAs and has the highest incidence of side effects and drug-drug interactions. Proton pump inhibitors (PPIs), act by blocking acid secretion at the hydrogen-potassium adenosine triphosphatase (H+, K+- ATPase) pump cited on the luminal border of the gastric parietal cell. Normally, this pump exchanges hydrogen for potassium across the parietal cell microvillus membrane; secreting hydrogen ions into the gastric lumen, thus, creating the low pH environment characteristic of gastric secretions. Proton pump inhibitors bind to and irreversibly inhibit the adenosine triphosphatase and are the most effective anti secretory agents and achieving better pH control. Gastric HCl affects PPIs and they become inactivated if permitted to dissolve in acidic gastric juice. The third group is prostaglandins; misoprostol (Cytotec) is a 15-deoxy-15-hydroxy-16-methyl analogue of prostaglandin E1. It has the same properties as other E-type prostaglandins, displaying moderate inhibition of basal and food-stimulated acid secretion in humans. Their main side effects are cramp-like abdominal pain and diarrhea, which are dose-dependent effects (Soll and Graham, 2008). 7.2 Eradication of H pylori infection The combination of a proton pump inhibitor, clarithromycin and amoxicillin or metronidazole seems successful especially if treatment extends for more than seven days (triple therapy). A sequential treatment regimen developed because of increased bacterial resistance, it consists of a proton pump inhibitor and amoxicillin for five days; followed by five additional days of a PPI, clarithromycin and tinidazole. 7.3 Recurring or a refractory peptic ulcer A refractory ulcer is usually more than 0.5 cm, resistant to PPI treatment for 6-8 weeks or H2RAs treatment or 8-10 weeks. In these cases a careful search for H pylori is highly recommended (Yuan et al, 2006). Consequently, with this discovery noted, it has been inferred that since the introduction of PPI drugs, the incidence of peptic ulcer disease complication has significantly decreased. On the other hand, it has also been said that eradication H. pylori infection is more efficient than anti secretory non-eradicating therapy in preventing recurrent bleeding from peptic ulcer. PROGNOSIS Upper gastrointestinal bleeding (haematemesis) occurs in nearly 15 to 20% of patients with peptic ulcer disease. It is the commonest indication for surgery. Perforation of a peptic ulcer, in duodenal ulcer, the risk of perforation is nearly 60% and is less in antral or lesser curvature ulcers. Perforation of a peptic ulcer leads to chemical and or bacterial peritonitis, which is a surgical emergency. Peptic ulcer disease causes gastric outlet obstruction in nearly 5 to 8% of cases; which develops as a result of inflammation, spasm, oedema, or scarring and fibrosis of the ulcer area. It is suspected with the onset of recurrent episodes of vomiting of large amounts containing undigested food. In long standing cases, hypochloraemic, hypoalkalaemic alkalosis occur with weight loss and dehydration. PREVENTION Since most peptic ulcers are caused by stomach upsetting medication, here is a table of suggestive reduction of effects of NSAID and aspirin that could affect to the prevention of peptic ulcer an individual needing the said medication. SOURCE: http://www.uspharmacist.com/CMSImagesContent/2008/12/USP0812%20NSAIDs%20T1.jpg. (July 17, 2009). Through this control of medicine intake, reduction of the development of peptic ulcer could then be handled successfully. REFERENCES: Shashidhar H, Flomenhoft D and Tolia V, 2009. Helicobacter pylori in pediatrics. Therapy, 6 1, 65-73. Soll AH and Graham DY, 2008. Approach to the patient with dyspepsia and peptic ulcer disease. In Yamada T, Alpers DH, Kalloo AN, Kaplowitz N, Owyang C and Powell DW, ed. Principles of Clinical Gastroenterology. Chichester, UK: Wiley-Blackwell, 2008. 99-121. Yuan Y, Padol IT and Hunt RH, 2006. Peptic Ulcer Disease Today. Nat Clin Pract Gastroenterol Hepatol, 3(2), 80-89. Preventing Peptic Ulcer. http://www.uspharmacist.com/CMSImagesContent/2008/12/USP0812%20NSAIDs%20T1.jpg. (July 17, 2009). Peptic Ulcer explained. :myhealth.ucsd.edu/.../topic.asphwid=tp12110 . (July 17, 2009). Kuipers EJ and Blaser MJ, 2007. Acid Peptic Disease: Epidemiology and Pathobiology (Chapter 141). In Ausiello DA and Goldman L, ed. Cecil Textbook of Medicine. 21st edition. St. Louis: Saunders, 2007. P. 1041 Liu YI, Wise PH and Butte AJ, 2009. The "etiome": identification and clustering of human disease etiological factors. BMC Bioinformatics, 10 (Suppl2), S14-S23. Read More