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| {{Infobox_Disease | | | {{Infobox_Disease | |
| Name = {{PAGENAME}} | | | Name = {{PAGENAME}} | |
| Image = Deep gastric ulcer.png | | | Image = Deep gastric ulcer.png | |
| Caption = Deep gastric ulcer | | | Caption = Deep gastric ulcer | |
| DiseasesDB = 9819 |
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| ICD10 = {{ICD10|K|25||k|20}}-{{ICD10|K|27||k|20}} |
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| ICD9 = {{ICD9|531}}-{{ICD9|534}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = |
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| eMedicineSubj = |
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| eMedicineTopic = |
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| eMedicine_mult = |
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| MeshID = D010437 |
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| }} | | }} |
| {{SI}} | | {{Peptic ulcer}} |
| '''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
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| {{CMG}} | | {{CMG}} ; {{AE}} {{MKK}} |
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| {{Editor Help}} | | {{SK}} Gastroduodenal ulcers; Peptic ulceration; gastric ulcer; duodenal ulcer. |
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| ==Overview== | | ==[[Peptic ulcer overview|Overview]]== |
| A '''peptic ulcer''', also known as '''[[PUD]]''' or '''[[peptic ulcer disease]]'''<ref name="medmag">{{cite web | url= http://www.emedmag.com/html/pre/gic/consults/071503.asp| title=GI Consult: Perforated Peptic Ulcer|accessdate=2007-08-26}}</ref> is an [[ulcer]] of an area of the [[gastrointestinal tract]] that is usually acidic and thus extremely painful. 80% of ulcers are associated with ''[[Helicobacter pylori]]'', a spiral-shaped bacterium that lives in the acidic environment of the stomach, however only 20% of those cases go to a doctor (for it is not a dangerous case if caught in time and can be treated with surgery). Ulcers can also be caused or worsened by drugs such as [[Aspirin]] and other [[NSAID]]s. Contrary to general belief, more peptic ulcers arise in the [[duodenum]] (first part of the [[small intestine]], just after the stomach) than in the [[stomach]]. About 4% of stomach ulcers are caused by a [[malignant]] tumor, so multiple biopsies are needed to make sure. Duodenal ulcers are generally [[benign]].
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| == Epidemiology == | | ==[[Peptic ulcer historical perspective|Historical Perspective]]== |
| In Western countries the [[prevalence]] of ''[[Helicobacter pylori]]'' [[infection]]s roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third world countries. Transmission is by food, contaminated groundwater, and through human saliva (such as from kissing or sharing food utensils.)
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| According to Mayo Clinic, however, there is no evidence that the infection can be transmitted by kissing:
| | ==[[Peptic ulcer classification|Classification]]== |
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| "No evidence indicates that this bacterial infection is transmitted by sharing food or kissing." (http://www.mayoclinic.org/peptic-ulcers/qanda.html))
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| A minority of cases of ''Helicobacter'' infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort, [[abdominal pain]] or [[gastritis]]. The prevalence of infection is greater in developing countries and is influenced by socioeconomic conditions, ethnic background and age. In the Philippines, there is scarcity of published data regarding the epidemiology
| | ==[[Peptic ulcer pathophysiology|Pathophysiology]]== |
| of this bacterium. Locally unpublished reports revealed a prevalence of 5.6% seropositivity rate in children and 60% among 136 adult Filipino patients with dyspepsia using the Clotest® (Cabahug et. al. 2003 and Caballero et al., 1997, unpublished data). A lower prevalence rate of
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| 42% was reported by Daez et. al. in 2002 (unpublished data) among 375 patients undergoing endoscopy at the Philippine General Hospital utilizing the rapid urease test and histopathology.
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| ==History== | | ==[[Peptic ulcer causes|Causes]]== |
| {{see also|Timeline of peptic ulcer disease and Helicobacter pylori}}
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| In 1997, the [[Centers for Disease Control and Prevention]], with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between ''[[H. pylori]]'' and ulcers. This campaign reinforced the news that ulcers are a curable infection, and the fact that health can be greatly improved and money saved by disseminating information about ''H. pylori''.<ref>[http://www.cdc.gov/ulcer/history.htm Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases]</ref>
| | ==[[Peptic ulcer differential diagnosis|Differentiating Peptic ulcer from other Diseases]]== |
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| ''[[Helicobacter pylori]]'' was rediscovered in 1982 by two Australian scientists [[Robin Warren]] and [[Barry Marshall]]<ref>{{cite journal|author=Marshall BJ|title=Unidentified curved bacillus on gastric epithelium in active chronic gastritis|journal=[[The Lancet|Lancet]]|year=1983|volume=1|issue=8336|pages=1273–1275|id=PMID 6134060}}</ref>. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by colonization with this bacterium, not by [[stress (medicine)|stress]] or [[spicy food]] as had been assumed before.<ref>{{cite journal|author=Marshall BJ, Warren JR|title=Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration|journal=Lancet|year=1984|volume=1|issue=8390|pages=1311–1315|id=PMID 6145023}}</ref>
| | ==[[Peptic ulcer epidemiology and demographics|Epidemiology and Demographics]]== |
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| The ''[[H. pylori]]'' hypothesis was poorly received, so in an act of self-experimentation Marshall drank a petri-dish containing a culture of organisms extracted from a patient and soon developed gastritis. His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria at the urging of his wife, since [[halitosis]] is one of the symptoms of infection.<ref name="mja">{{cite web | url= http://www.mja.com.au/public/issues/183_11_051205/van11000_fm.html#0_i1091639| title=Research Enterprise, The 2005 Nobel Prize in Physiology or Medicine |accessdate=2007-08-26}}</ref> This experiment was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal.
| | ==[[Peptic ulcer risk factors|Risk Factors]]== |
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| In 2005, the Karolinska Institute in Stockholm awarded the [[Nobel Prize in Physiology or Medicine]] to Dr. Marshall and his long-time collaborator Dr. [[Robin Warren|Warren]] "for their discovery of the bacterium ''Helicobacter pylori'' and its role in [[gastritis]] and peptic ulcer disease". Professor Marshall continues research related to ''H. pylori'' and runs a molecular biology lab at UWA in Perth, Western Australia.
| | ==[[Peptic ulcer screening|Screening]]== |
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| ==Classification== | | ==[[Peptic ulcer natural history|Natural History, Complications and Prognosis]]== |
| [[Image:Benign gastric ulcer 1.jpg|thumb|left|200px|A benign gastric ulcer (from the antrum) of a [[gastrectomy]] specimen.]] | |
| <!-- [[Image:Gastric ulcer 3.jpg|left|thumb|200px|Endoscopic image of gastric ulcer, biopsy proven to be [[gastric cancer]].]] -->
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| A peptic ulcer may arise at various locations:
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| * [[Stomach]] (called '''gastric ulcer''')
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| * [[Duodenum]] (called '''duodenal ulcer''')
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| * [[Esophagus]] (called '''esophageal ulcer''')
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| * [[Meckel's diverticulum]]
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| | | ==[[Peptic ulcer diagnosis|Diagnosis]]== |
| | | [[Peptic ulcer history and symptoms|History and Symptoms]] | [[Peptic ulcer physical examination|Physical Examination]] | [[Peptic ulcer Echocardiogram|Echocardiogram]] | [[Peptic ulcer laboratory tests|Laboratory Findings]] | [[Peptic ulcer x ray| X Ray]] | [[Peptic ulcer CT|CT]] | [[Peptic ulcer ultrasound|Ultrasound]] | [[Peptic ulcer other imaging findings|Other Imaging Findings]] | [[Peptic ulcer other diagnostic studies|Other Diagnostic Studies]] |
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| ==Signs and symptoms==
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| Symptoms of a peptic ulcer can be:
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| * [[Abdominal pain]], classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
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| * Bloating and abdominal fullness
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| * Waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus)
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| * Nausea, and lots of vomiting
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| * Loss of appetite and weight loss;
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| * [[Hematemesis]] (vomiting of blood); if the blood is just streaks, then the esophagus probably got hurt from all the vomitting.
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| * [[Melena]] (tarry, foul-smelling faeces due to [[oxidation|oxidized]] iron from [[hemoglobin]])
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| * Rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.
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| A history of [[heartburn]], [[gastroesophageal reflux disease]] (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include [[NSAID]] (non-steroid anti-inflammatory drugs) that inhibit [[cyclooxygenase]], and most [[glucocorticoid]]s (e.g. [[dexamethasone]] and [[prednisolone]]).
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| In patients over 45 with more than 2 weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).
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| The timing of the symptoms in relation to the meal may differentiate between ''gastric'' and ''duodenal ulcers'': A gastric ulcer would give epigastric pain ''during'' the meal, as [[gastric acid]] is secreted, or ''after'' the meal, as the alkaline duodenal contents reflux into the [[stomach]]. Symptoms of duodenal ulcers would manifest mostly ''before'' the meal — when acid (production stimulated by hunger) is passed into the [[duodenum]]. However, this is not a reliable sign in clinical practice.
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| ==Stress and ulcers==
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| Despite the finding that a [[bacterial infection]] is the cause of ulcers in 80% of cases, [[bacterial infection]] does not appear to explain all ulcers and researchers continue to look at stress as a possible cause, or at least a complication in the development of ulcers.
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| An expert panel convened by the Academy of Behavioral Medicine research concluded that ulcers are not purely an [[infectious disease]] and that psychological factors do play a significant role.<ref name="medmag"/> Researchers are examining how stress might promote ''H. pylori'' infection. For example, ''Helicobacter pylori'' thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid.
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| The discovery that ''Helicobacter pylori'' is a cause of peptic ulcer has tempted many to conclude that psychological factors are unimportant. But this is dichotomised thinking. There is solid evidence that psychological stress triggers many ulcers and impairs response to treatment, while helicobacter is inadequate as a monocausal explanation as most infected people do not develop ulcers. Psychological stress probably functions most often as a cofactor with ''H pylori''. It may act by stimulating the production of [[gastric acid]] or by promoting behavior that causes a risk to health. Unravelling the aetiology of peptic ulcer will make an important contribution to the biopsychosocial model of disease.<ref name="bmj">{{cite web | url= http://bmj.bmjjournals.com/cgi/content/full/316/7130/538| title=Stress and peptic ulcer: life beyond helicobacter|accessdate=2007-08-26}}</ref>
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| A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor (PMID 12948263).
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| A study on mice showed that both long-term water-immersion-restraint stress and ''H. pylori'' infection were independently associated with the development of peptic ulcers (PMID 12465722).
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| == Pathophysiology ==
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| [[Tobacco smoking]], [[Blood type|blood group]], spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.<ref>For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids. [http://digestive.niddk.nih.gov/ddiseases/pubs/hpylori/ National Digestive Diseases Information Clearinghouse]</ref> | |
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| A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic [[inflammation]] due to ''[[Helicobacter pylori]]'' that colonizes (''i.e.'' settles there after entering the body) the [[Pyloric antrum|antral]] [[mucosa]]. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the [[bacterium]] can cause a chronic active [[gastritis]] (type B gastritis), resulting in a defect in the regulation of [[gastrin]] production by that part of the stomach, and gastrin secretion is increased. [[Gastrin]], in turn, stimulates the production of [[gastric acid]] by parietal cells. The acid erodes the [[mucosa]] and causes the ulcer.
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| Another major cause is the use of [[NSAID]]s (see above). The gastric mucosa protects itself from [[gastric acid]] with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of [[cyclooxygenase]] 1 (''cox-1''), which is essential for the production of these prostaglandins. Newer NSAIDs ([[celecoxib]], [[rofecoxib]]) only inhibit ''cox-2'', which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.
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| [[Glucocorticoid]]s lead to atrophy of all [[epithelium|epithelial]] tissues. Their role in ulcerogenesis is relatively small.
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| There is debate as to whether ''Stress'' in the psychological sense can influence the development of peptic ulcers (see Stress and ulcers above). [[Burn (injury)|Burns]] and [[head trauma]], however, can lead to "stress ulcers", and it is reported in many patients who are on [[mechanical ventilation]].
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| [[Tobacco smoking|Smoking]] leads to [[atherosclerosis]] and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through [[ischemia]].
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| Overuse of laxatives is also known to cause peptic ulcers.
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| A [[Family history (medicine)|family history]] is often present in duodenal ulcers, especially when [[ABO blood group system|blood group O]] is also present. Inheritance appears to be unimportant in gastric ulcers.
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| [[Gastrinoma]]s ([[Zollinger-Ellison syndrome]]), rare gastrin-secreting tumors, cause multiple and difficult to heal ulcers. | |
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| == Diagnosis ==
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| An [[esophagogastroduodenoscopy]] ([[EGD]]), a form of [[endoscopy]], also known as a [[gastroscopy]], is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
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| The diagnosis of ''[[Helicobacter pylori]]'' can be by:
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| *Breath testing (does not require EGD);
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| *Direct culture from an EGD biopsy specimen;
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| *Direct detection of [[urease]] activity in a biopsy specimen;
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| *Measurement of [[antibody]] levels in [[blood]] (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy.
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| The possibility of other causes of ulcers, notably [[malignancy]] ([[gastric cancer]]) needs to be kept in mind. This is especially true in ulcers of the ''greater (large) curvature'' of the [[stomach]]; most are also a consequence of chronic ''H. pylori'' infection.
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| If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.
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| ===Macroscopical appearance===
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| Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular as in the ulcerative form of gastric cancer. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
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| ===Microscopical appearance===
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| A gastric peptic ulcer is a mucosal defect which penetrates the [[muscularis mucosae]] and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.<ref name="pathologyatlas">{{cite web | url= http://www.pathologyatlas.ro/Peptic%20ulcer.html| title=ATLAS OF PATHOLOGY|accessdate=2007-08-26}}</ref>
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| == Differential Diagnosis ==
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| *Alcohol
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| *[[Alpha-1 Antitrypsin Deficiency]]
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| *Basophilic leukemia
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| *[[Burn]]s
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| *Cerebral [[trauma]]
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| *Chronic debilitated conditions
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| *[[Chronic obstructive pulmonary disease]]
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| *[[Chronic Renal Failure]]
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| *Cigarette smoking
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| *[[Cirrhosis]]
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| *[[Cystic Fibrosis]]
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| *Glucosteroids
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| *[[Helicobacter pylori infection]]
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| *[[Hyperparathyroidism]]
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| *Incompetant gastroesophageal sphincter
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| *[[NSAID]]s
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| *Severe systemic disease
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| *[[Zollinger-Ellison Syndrome]]
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| ==Treatment== | | ==Treatment== |
| | [[Peptic ulcer medical therapy|Medical Therapy]] | [[Peptic ulcer surgery|Surgery]] | [[Peptic ulcer primary prevention|Primary Prevention]] | [[Peptic ulcer secondary prevention|Secondary Prevention]] | [[Peptic ulcer cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Peptic ulcer future or investigational therapies|Future or Investigational Therapies]] |
| | ==Case Studies== |
| | [[Peptic ulcer case study one|Case #1]] |
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| Younger patients with ulcer-like symptoms are often treated with [[antacid]]s or [[H2 antagonist]]s before EGD is undertaken. [[Bismuth subsalicylate|Bismuth compounds]] may actually reduce or even clear organisms.
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| Patients who are taking [[NSAIDs|nonsteroidal anti-inflammatories]] (NSAIDs) may also be prescribed a [[prostaglandin]] [[analog (chemistry)|analogue]] ([[Misoprostol]]) in order to help prevent peptic ulcers, which may be a side-effect of the NSAIDs.
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| When ''H. pylori'' infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. [[Erythromycin]], [[Ampicillin]], [[Amoxicillin]], [[Tetracycline]], [[Metronidazole]]) and 1 [[proton pump inhibitor]] (PPI). An effective combination would be [[Amoxicillin]] + [[Metronidazole]] + [[Pantoprazole]] (a PPI). In the absence of ''H. pylori'', long-term higher dose PPIs are often used.
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| Treatment of ''H. pylori'' usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective [[vagotomy]]") for uncomplicated peptic ulcers became obsolete.
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| Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cauterizations or injection.
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| ==Complications==
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| *'''[[Upper gastrointestinal bleeding|Gastrointestinal bleeding]]''' is the commonest complication. Sudden large bleeding can be life threatening<ref name="pmid9391242">{{cite journal |author=Cullen DJ, Hawkey GM, Greenwood DC, ''et al'' |title=Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs |journal=Gut |volume=41 |issue=4 |pages=459–62 |year=1997 |pmid=9391242 |doi=}}</ref>. It occurs when the ulcer erodes one of the blood vessels.
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| *'''Perforation''' (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity. Perforation at the anterior surface of stomach leads to acute [[peritonitis]], initially chemical and later bacterial peritonitis. Often first sign is sudden intense abdominal pain. Posterior wall perforation leads to [[pancreatitis]]; pain in this situation often radiates to back.
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| *'''Penetration''' is when the ulcer continues into adjacent organs such as liver and [[pancreas]]<ref>{{cite web |url=http://www.merck.com/mmhe/sec09/ch121/ch121c.html |title=Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition |accessdate=2007-10-10 |format= |work=}}</ref>.
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| *Scarring and swelling due to ulcers causes narrowing in the duodenum and '''[[gastric outlet obstruction]]'''. Patient often presents with severe vomiting.
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| ==References==
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| {{reflist|2}}
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| == External links ==
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| *[http://www.pathologyatlas.ro/Peptic%20ulcer.html Pathology specimen of Gastric ulcer]
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| *[http://www.surgeons.org.uk/general-surgery/perforated-duodenal-ulceration.html A case report and tutorial on perforated duodenal ulcer]
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| *[http://www.peptic-ulcers.co.uk/causes.html Causes of Peptic ulcers]
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| {{SIB}}
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| {{Gastroenterology}} | | {{Gastroenterology}} |
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| [[Category:Gastroenterology]]
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| [[Category:Abdominal pain]]
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| [[bs:Ulcerozne lezije želuca]] | | [[bs:Ulcerozne lezije želuca]] |
| [[ca:Úlcera pèptica]] | | [[ca:Úlcera pèptica]] |
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