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Peptic ulcer disease

Deep gastric ulcer

Classification and external resources

Specialty Gastroenterology, general surgery

ICD-10 K25

(http://apps.who.int/classifications/icd10/browse/2015/en#/K25)–K

(http://apps.who.int/classifications/icd10/browse/2015/en#/K27)

ICD-9-CM 531 (http://www.icd9data.com/getICD9Code.ashx?icd9=531)–534

(http://www.icd9data.com/getICD9Code.ashx?icd9=534)

DiseasesDB 9819 (http://www.diseasesdatabase.com/ddb9819.htm)

MedlinePlus 000206

(http://www.nlm.nih.gov/medlineplus/ency/article/000206.htm)

eMedicine med/1776 (http://www.emedicine.com/med/topic1776.htm) ped/23

(http://www.emedicine.com/ped/topic2341.htm#)

MeSH D010437 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?

field=uid&term=D010437)

Peptic ulcerFrom Wikipedia, the free encyclopedia

Peptic ulcer disease (PUD), also

known as a peptic ulcer or

stomach ulcer, is a break in the

ining of the stomach, first part of he small intestine, or

occasionally the lower

esophagus.[1][2] An ulcer in the

stomach is known as a gastric

ulcer while that in the first part of 

he intestines is known as a

duodenal ulcer. The most

common symptoms are waking at

night with upper abdominal pain

or upper abdominal pain thatmproves with eating. The pain is

often described as a burning or

dull ache. Other symptoms

nclude belching, vomiting,

weight loss, or poor appetite.

About a third of older people

have no symptoms.[1]

Complications may include

bleeding, perforation, and

blockage of the stomach.Bleeding occurs in as many as

15% of people.[3]

Common causes include the

bacteria, Helicobacter pylori and

non-steroidal anti-inflammatory

drugs (NSAIDs).[1] Other less

common causes include tobacco

smoking, stress due to serious

llness, Behcet disease, Zollinger-Ellison syndrome, Crohn disease and liver cirrhosis, among others.[1][4] Ol

people are more sensitive to the ulcer causing effects of NSAIDs. The diagnosis is typically suspected due to

presenting symptoms with confirmation by either endoscopy or barium swallow. H. pylori can be diagnosed

esting the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the

stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, an

nflammation of the stomach lining or gallbladder.[1]

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Diet does not play an important role in either causing or preventing ulcers.[5] Treatment includes stopping

smoking, stopping NSAIDs, stopping alcohol, and medications to decrease stomach acid. The medication us

o decrease acid is usually either a proton pump inhibitor (PPI) or an H2 blocker with four weeks of treatmen

nitially recommended.[1] Ulcers due to H. pylori are treated with a combination of medications such as

amoxicillin, clarithromycin, and a PPI. Antibiotic resistance is increasing and thus treatment may not always

effective.[6] Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in

which it is not successful.[3]

Peptic ulcers are present in around 4% of the population.[1] About 10% of people develop a peptic ulcer at so

point in their life.[7] They resulted in 301,000 deaths in 2013 down from 327,000 deaths in 1990. [8] The first

description of a perforated peptic ulcer was in 1670 in Princess Henrietta of England.[3]  H. pylori was first

dentified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century,[6] a discover

for which they received the Nobel Prize in 2005.[9]

Contents

1 Signs and symptoms1.1 Complications

2 Cause2.1 H. pylori2.2 NSAIDs2.3 Stress2.4 Diet2.5 Other

3 Diagnosis3.1 Classification3.2 Macroscopic appearance3.3 Microscopic appearance3.4 Differential diagnosis

4 Treatment4.1 Acid reducing medication4.2 H. pylori4.3 Surgery

5 Epidemiology

6 History7 Notes8 References9 External links

Signs and symptoms

Signs and symptoms of a peptic ulcer can include one or more of the following:

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abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers thepain appears about three hours after taking a meal;bloating and abdominal fullness;waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this more associated with gastroesophageal reflux disease);nausea, and copious vomiting;loss of appetite and weight loss;hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from

damage to the esophagus from severe/continuing vomiting.melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme,

stabbing pain,[10] and requires immediate surgery.

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 NSAIDs (non-steroid anti

nflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and

prednisolone).

n patients over 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are highenough to warrant rapid investigation by esophagogastroduodenoscopy.

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 production is increased as food enter

he stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter clo

o concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would

manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the

duodenum.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the patient's age. Furthermor

ypical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wan

disappear.[11] Usually, children and the elderly do not develop any symptoms unless complications have aris

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly

accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caus

by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area

The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few

minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flar

night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti

acid medication.[12]

 However, peptic ulcer disease symptoms may be different for every sufferer.[13]

Complications

Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-

threatening.[14] It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenalartery.Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if untreated. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal

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content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute

peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intenseabdominal pain; an example is Valentino's syndrome, named after the silent-film actor who experiencethis pain before his death. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum.Perforation and penetration are when the ulcer continues into adjacent organs such as the liver and

pancreas.[11]

Gastric outlet obstruction is the narrowing of pyloric canal by scarring and swelling of gastric antrum duodenum due to peptic ulcers. Patient often presents with severe vomiting without bile.Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the

etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.[11]

Cause

H. pylori

A major causative factor (60% of gastric and up to 50-75%[15] of duodenal ulcers) is chronic inflammation d

o Helicobacter pylori that colonizes the antral mucosa.[16] The immune system is unable to clear the infectio

despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastriti

Gastrin stimulates the production of gastric acid by parietal cells. In H. pylori colonization responses to

ncreased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formati

NSAIDs

Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer o

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. COX-2 selective antnflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is les

essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

Stress

Stress due to serious health problems such as those requiring treatment in an intensive care unit is well

described as a cause of peptic ulcers, which are termed stress ulcers.[4]

While chronic life stress was once believed to be the main cause of ulcers this is no longer the case.[17] It is,

however, still occasionally believed to play a role.[17] This may be by increasing the risk in those with other

causes such as H. pylori or NSAID use.[18]

Diet

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Endoscopic image of gastric ulcer,

biopsy proven to be gastric cancer.

Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, b

have been shown to be of relatively minor importance.[19] Caffeine and coffee, also commonly thought to ca

or exacerbate ulcers, appear to have little effect.[20][21] Similarly, while studies have found that alcohol

consumption increases risk when associated with H. pylori infection, it does not seem to independently incre

risk. Even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk

factor.[22][23][nb 1]

Other

Although some studies have found correlations between smoking and ulcer formation,[24] others have been

more specific in exploring the risks involved and have found that smoking by itself may not be much of a ris

factor unless associated with H. pylori infection.[22][25][26][nb 2]

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to

heal ulcers.

Diagnosis

The diagnosis is mainly established based on the characteristic

symptoms. Stomach pain is usually the first signal of a peptic ulcer. In

some cases, doctors may treat ulcers without diagnosing them with

specific tests and observe whether the symptoms resolve, thus indicating

hat their primary diagnosis was accurate.

Confirmation of the diagnosis is made with the help of tests such as

endoscopies or barium contrast x-rays. The tests are typically ordered if 

he symptoms do not resolve after a few weeks of treatment, or when

hey first appear in a person who is over age 45 or who has other

symptoms such as weight loss, because stomach cancer can cause

similar symptoms. Also, when severe ulcers resist treatment, particularly

f a person has several ulcers or the ulcers are in unusual places, a doctor

may suspect an underlying condition that causes the stomach to

overproduce acid.[11]

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out o

patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ul

can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their

nability to differentiate between past exposure to the bacteria and current infection. Additionally, a false

negative result is possible with a blood test if the patient has recently been taking certain drugs, such as

antibiotics or proton pump inhibitors.[27]

The diagnosis of Helicobacter pylori can be made by:

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1. Esophagus

2. Stomach

3.Ulcers4.Duodenum

5.Mucosa

6.Submucosa

7.Muscle

Urea breath test (noninvasive and does not require EGD);Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs anot set up to perform H. pylori cultures;Direct detection of urease activity in a biopsy specimen by rapid urease test;Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversialwhether a positive antibody without EGD is enough to warrant eradication therapy;Stool antigen test;Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon to detect H. pylori.[28] To perform this exam the patient will be asked

drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. Afte

an hour, the patient will be asked to blow into a bag that is sealed. If the patient is infected with H. pylori, the

breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to mon

he response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This

especially true in ulcers of the greater (large) curvature of the stomach; most are also a consequence of chro

H. pylori infection.

f 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

ateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

Classification

By area

Duodenum (called duodenal ulcer)Esophagus (called esophageal ulcer)Stomach (called gastric ulcer)Meckel's diverticulum (called Meckel's diverticulum ulcer; is verytender with palpation)

Modified Johnson

Type I: Ulcer along the body of the stomach, most often along the

lesser curve at incisura angularis along the locus minorisresistantiae. Not associated with acid hypersecretion.Type II: Ulcer in the body in combination with duodenal ulcers.Associated with acid oversecretion.Type III: In the pyloric channel within 3 cm of pylorus.Associated with acid oversecretion.Type IV: Proximal gastroesophageal ulcerType V: Can occur throughout the stomach. Associated with chronic use of NSAIDs (such as ibuprofe

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A benign gastric ulcer (from the

antrum) of a gastrectomy specimen

Macroscopic appearance

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 in the acute form of peptic ulcer, regular but

with elevated borders and inflammatory surrounding in the chronic form.

n the ulcerative form of gastric cancer the borders are irregular.Surrounding mucosa may present radial folds, as a consequence of the

parietal scarring.

Microscopic appearance

A gastric peptic ulcer is a mucosal defect which penetrates the

muscularis mucosae and lamina 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:

nflammatory exudate, fibrinoid necrosis, granulation tissue and fibrousissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.[29]

Differential diagnosis

GastritisStomach cancerGastroesophageal reflux diseasePancreatitisHepatic congestion

CholecystitisBiliary colicInferior myocardial infarctionReferred pain (pleurisy, pericarditis)Superior mesenteric artery syndrome

Treatment

Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscop

s undertaken.

People who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin

analogue (misoprostol) in order to help prevent peptic ulcers.

Acid reducing medication

Ranitidine and famotidine, which are both H2 antagonists, provide relief of peptic ulcers, heartburn, indigest

They decrease the amount of acid in the stomach helping with healing of ulcers.[30]

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n the absence of H. pylori, 4 weeks of a PPIs are also often used.

H. pylori

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g.

clarithromycin, amoxicillin, tetracycline, metronidazole) and a proton pump inhibitor (PPI), sometimes toget

with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin +

clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. Aeffective first-line therapy for uncomplicated cases would be amoxicillin + metronidazole + pantoprazole (a

PPI).

Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulce

Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since

widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplica

peptic ulcers became obsolete.

Surgery

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding

ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.

Epidemiology

The lifetime risk for developing a peptic ulcer is approximately 10%.[7] They resulted in 301,000 deaths in 2

down from 327,000 deaths in 1990.[8]

n Western countries the percentage of people with Helicobacter pylori infections 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 where it is

estimated at about 70% of the population, whereas developed countries show a maximum of 40% ratio. Over

H. pylori infections show a worldwide decrease, more so in developed countries. Transmission is by food,

contaminated groundwater, and through human saliva (such as from kissing or sharing food utensils).[32]

A minority of cases of H. pylori infection will eventually lead to an ulcer and a larger proportion of people w

get non-specific discomfort, abdominal pain or gastritis.

Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of the 20th

century, when epidemiological trends started to point to an impressive fall in its incidence.[33]

 The reason thahe rates of peptic ulcer disease decreased is thought to be the development of new effective medication and

acid suppressants and the discovery of the cause of the condition, H. pylori.

The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of 

gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in

ncidence is considered to be a cohort-phenomenon independent of the progress in treatment of the disease. T

cohort-phenomenon is probably explained by improved standards of living which has lowered the incidence

H. pylori infections.[34]

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Disability-adjusted life year for pep

ulcer disease per 100,000 inhabitan

in 2004.[31]

  no data

  less than 20

  20–40

  40–60

  60–80

  80–100

  100–120

  120–140

  140–160

  160–180

  180–200

  200–220

  more than 220

History

John Lykoudis, a general practitioner in Greece, treated patients for

peptic ulcer disease with antibiotics, beginning in 1958, long before it

was commonly recognized that bacteria were a dominant cause for the

disease.[35]

Helicobacter pylori was identified in 1982 by two Australian scientists,

Robin Warren and Barry J. Marshall as a causative factor for ulcers.[36]

n their original paper, Warren and Marshall contended that most gastric

ulcers and gastritis were caused by colonization with this bacterium, not

by stress or spicy food as had been assumed before.[37]

The H. pylori hypothesis was initially poorly received,[38] so in an act of 

self-experimentation Marshall drank a Petri dish containing a culture of 

organisms extracted from a patient and five days later developed

gastritis. His symptoms disappeared after two weeks, but he tookantibiotics to kill the remaining bacteria at the urging of his wife, since

halitosis is one of the symptoms of infection.[39] This experiment was

published in 1984 in the Australian Medical Journal and is among the

most cited articles from the journal.

n 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 that health can be greatly improved and money saved by disseminating information ab

H. pylori.[40]

n 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr.

Marshall and his long-time collaborator Dr. Warren "for their discovery of the bacterium Helicobacter pylor

and its role in gastritis and peptic ulcer disease." Professor Marshall continues research related to H. pylori a

runs a molecular biology lab at UWA in Perth, Western Australia.

Some believed that mastic gum, a tree resin extract, actively eliminates the H. pylori bacteria.[41] However,

multiple subsequent studies have found no effect of using mastic gum on reducing H. pylori levels.[42][43]

Notes

1. Sonnenberg in his study cautiously concludes that, among other potential factors that were found to correlate to ulcer

healing, "moderate alcohol intake might [also] favor ulcer healing." (p. 1066)

2. Kurata 1997 explains that "Data in Fig. 8 indicate that 89% of all serious upper GI disease can be accounted for by

NSAIDs and H. pylori, with cigarette smoking acting as a synergistic co-factor."(14)

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2. "Definition and Facts for Peptic Ulcer Disease" (http://www.niddk.nih.gov/health-information/health-topics/digestive

diseases/peptic-ulcer/Pages/definition-facts.aspx). http://www.niddk.nih.gov/ . Retrieved 28 February 2015.

3. Milosavljevic, T; Kosti!-Milosavljevi!, M; Jovanovi!, I; Krsti!, M (2011). "Complications of peptic ulcer disease.".

 Digestive diseases (Basel, Switzerland) 29 (5): 491–3. doi:10.1159/000331517

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4. Steinberg, KP (June 2002). "Stress-related mucosal disease in the critically ill patient: risk factors and strategies to

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5. "Eating, Diet, and Nutrition for Peptic Ulcer Disease" (http://www.niddk.nih.gov/health-information/health-

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6. Wang, AY; Peura, DA (October 2011). "The prevalence and incidence of Helicobacter pylori-associated peptic ulcer

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nobelprize.org. Nobel Media AB. Retrieved 3 June 2015.

10. Bhat, Sriram (2013). SRB's Manual of Surgery. p. 364. ISBN 9789350259443

11. "Peptic Ulcer" (http://www.merckmanuals.com/home/digestive_disorders/peptic_disorders/peptic_ulcer.html). Home

 Health Handbook for Patients & Caregivers. Merck Manuals. October 2006.12. "Peptic ulcer" (http://www.mayoclinic.com/health/peptic-ulcer/ds00242/dsection=symptoms). Retrieved 18 June 201

13. "Ulcer Disease Facts and Myths" (http://www.ulcerdisease.net/). Retrieved 18 June 2010.

14. Cullen DJ, Hawkey GM, Greenwood DC, et al. (1997). "Peptic ulcer bleeding in the elderly: relative roles of 

Helicobacter pylori and non-steroidal anti-inflammatory drugs" (http://gut.bmj.com/cgi/pmidlookup?

view=long&pmid=9391242). Gut  41 (4): 459–62. doi:10.1136/gut.41.4.459

(https://dx.doi.org/10.1136%2Fgut.41.4.459). PMC 1891536 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC18915

PMID 9391242 (https://www.ncbi.nlm.nih.gov/pubmed/9391242).

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article7501). web.archive.org. Retrieved 27 February 2014.

17. Fink, G (February 2011). "Stress controversies: post-traumatic stress disorder, hippocampal volume, gastroduodenalulceration*.". Journal of neuroendocrinology 23 (2): 107–17. doi:10.1111/j.1365-2826.2010.02089.x

(https://dx.doi.org/10.1111%2Fj.1365-2826.2010.02089.x). PMID 20973838

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External links

Gastric Ulcer (http://rad.usuhs.edu/medpix/parent.php3?mode=pt_finder&srchstr=gastric%20ulcer#top)

Approach to acute upper gastrointestinal bleeding in adults(Wolters Kluwer UpToDate)(http://www.uptodate.com/contents/approach-to-acute-upper-gastrointestinal-bleeding-in-adults)(MCQs on Peptic ulcer ) (http://www.mcqsurgery.com/ulcer)

Radiology and Endoscopy from MedPix

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