akk peptic ulcer

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A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer

disease,[1] is an ulcer (defined as mucosal erosions equal to or greater

than 0.5 cm) of an area of thegastrointestinal tract that is usually acidic and

thus extremely painful. As many as 70-90% of ulcers are associated

with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidicenvironment of the stomach, however only 40% of those cases go to a

doctor. Ulcers can also be caused or worsened by drugs such

as aspirin and otherNSAIDs.

Contrary to general belief, more peptic ulcers arise in the duodenum (first

part of the small intestine, just after the stomach) rather than in

the stomach. About 4% of stomach ulcers are caused by

a malignant tumor, so multiple biopsies are needed to exclude cancer.

Duodenal ulcers are generally benign.

Contents

[hide]

1 Classification

2 Signs and symptoms

2.1 Complications

3 Cause

3.1 Stress

4 Diagnosis

4.1 Macroscopic appearance

4.2 Microscopic appearance

4.3 Differential diagnosis of

epigastric pain

5 Treatment

6 Epidemiology

7 History

8 Notes

9 References 10 External links

[edit]Classification Stomach (called gastric ulcer)

Duodenum (called duodenal ulcer)

Oesophagus (called Oesophageal ulcer)
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Meckel's Diverticulum (called Meckel's

Diverticulum ulcer)

Types of peptic ulcers:

Type I: Ulcer along the lesser curve of stomach

Type II: Two ulcers present - one gastric, oneduodenal

Type III: Prepyloric ulcer

Type IV: Proximal gastroesophageal ulcer

Type V: Anywhere

[edit]Signs and symptomsSymptoms of a peptic ulcer can be

abdominal pain, classically epigastric with severity

relating to mealtimes, after around 3 hours oftaking a meal (duodenal ulcers are classically

relieved by food, while gastric ulcers are

exacerbated by it);

bloating and abdominal fullness;

waterbrash (rush of saliva after an episode of

regurgitation to dilute the acid in esophagus);

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 oxidized iron from hemoglobin);

rarely, an ulcer can lead to a gastric or

duodenal perforation, which leads to acute

peritonitis. This is extremely painful and requiresimmediate 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 NSAID (non-steroid anti-
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inflammatory drugs) that inhibit cyclooxygenase, and

most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the

odds for peptic ulceration are high enough to warrant rapid investigation by

EGD (see below).The timing of the symptoms in relation to the meal may differentiate

between gastricand duodenal ulcers: A gastric ulcer would

giveepigastric pain duringthe meal, as gastric acid is secreted, or afterthe

meal, as the alkaline duodenal contents reflux into thestomach. Symptoms

of duodenal ulcers would manifest mostly beforethe mealwhen acid

(production stimulated by hunger) is passed into the duodenum. However,

this is not a reliable sign in clinical practice.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer

and the patient's age. Furthermore, typical ulcers tend to heal and recur

and as a result the pain may occur for few days and weeks and then wane

or disappear. [2] Usually, children and theelderly do not develop any

symptoms unless complications have arisen.

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 caused

by the ulcer but it may aggravated by the stomach acidwhen it comes into

contact with the ulcerated area. The pain caused by peptic ulcers can befelt anywhere from the navel up to thebreastbone, it may last from few

minutes to several hours and it may be worse when the stomach is empty.

Also, sometimes the pain may flare at night and it can commonly be

temporarily relived by eating foods that buffer stomach acid or by taking

anti-acid medication. [3] However, peptic ulcer disease symptoms may be

different for every sufferer. [4]

[edit]Complications

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

threatening.[5] It occurs when the ulcer erodes one

of the blood vessels.

Perforation (a hole in the wall) often leads to

catastrophic consequences. Erosion of the gastro-
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intestinal wall by the ulcer leads to spillage of

stomach or intestinal content into the abdominal

cavity. Perforation at the anterior surface of the

stomach leads to acuteperitonitis, initially chemical

and later bacterial peritonitis. The first sign is oftensudden intense abdominal pain. Posterior wall

perforation leads to pancreatitis; pain in this

situation often radiates to the back.

Penetration is when the ulcer continues into

adjacent organs such as the liver and pancreas.[6]

Scarring and swelling due to ulcers causes

narrowing in the duodenum and gastric outlet

obstruction. Patient often presents with severe

vomiting.

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.[7]

[edit]CauseA major causative factor (60% of gastric and up to 90% of duodenal ulcers)

is chronic inflammation due to Helicobacter

pylorithatcolonizes the antralmucosa. The immune system is unable to

clear the infection, despite the appearance of antibodies. Thus,

thebacterium 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 can either be decreased (most cases)

resulting in hypo- or achlorhydria or increased. Gastrinstimulates the

production of gastric acid by parietal cells and, in H. pylori colonization

responses that increase gastrin, the increase in acid can contribute to the

erosion of the mucosa and therefore ulcer formation.Another major cause is the use of NSAIDs (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. COX-2 selective anti-inflammatories (such as celecoxib or
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the since withdrawnrofecoxib) preferentially inhibit cox-2, which is less

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

related gastric ulceration. As the prevalence of H. pylori-caused ulceration

declines in the Western world due to increased medical treatment, a

greater proportion of ulcers will be due to increasing NSAID use amongindividuals with pain syndromes as well as the growth of aging populations

that develop arthritis.

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 incidence is

considered to be a cohort-phenomenon independent of the progress in

treatment of the disease. The cohort-phenomenon is probably explained

by improved standards of living which has lowered the incidence of H.

pyloriinfections.[8]

Although some studies have found correlations between smoking and ulcer

formation [9], others have been more specific in exploring the risks involved

and have found that smoking by itself may not be much of a risk factor

unless associated with H. pyloriinfection[10][11][12][nb 1]. Some suggested risk

factors such as diet, spice, consumption and blood type, were

hypothesized as ulcerogens (helping cause ulcers) until late in the 20th

century, but have been shown to be of relatively minor importance in the

development of peptic ulcers.[13]. Similarly, while studies have found thatalcohol consumption increases risk when associated with H.

pyloriinfection, it does not seem to independently increase risk, and even

when coupled with H. pyloriinfection, the increase is modest in comparison

to the primary risk factor [10][14][nb 2].

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors,

also cause multiple and difficult to heal ulcers.

[edit]Stress

Researchers also continue to look at stress as a possible cause, or at leastcomplication, in the development of ulcers. There is debate as to whether

psychological stress can influence the development of peptic

ulcers. Burns and head trauma, however, can lead to physiologic stress

ulcers, which are reported in many patients who are on mechanical

ventilation.
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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.[1] Researchers are

examining how stress might promote H. pyloriinfection. For

example, Helicobacter pylorithrives in an acidic environment, and stresshas been demonstrated to cause the production of excess stomach acid.

This was supported by a study on mice showing that both long-term water-

immersion-restraint stress and H. pyloriinfection were independently

associated with the development of peptic ulcers.[15]

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.[16]

[edit]Diagnosis

Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.

The diagnosis is mainly established based on the characteristic symptoms.

The stomach pain is usually the first to signal a peptic ulcer. In somecases, doctors may treat ulcers without diagnosing them with specific tests

and observe if the symptoms resolve, meaning their primary diagnosis was

accurate.

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

endoscopies or barium contrast x-rays. The tests are typically ordered if
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the symptoms do not resolve after a few weeks of treatment, or when they

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 if a

person has several ulcers or the ulcers are in unusual places, a doctor maysuspect an underlying condition that causes the stomach to

overproduce acid.[17]

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also

known as agastroscopy, 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.

One of the reasons why blood tests are not reliable on establishing an

accurate peptic ulcer diagnosis on their own is their inability to differentiate

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

false-negative is possible with a blood test if the patient has recently been

taking certain drugs, such as antibiotics or proton pump inhibitors. [18]

The diagnosis of Helicobacter pylorican be made by:

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 labsare not set up to perform H. pyloricultures;

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 controversial

whether 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 atom to detect H. pylori. [19] To

perform this exam the patient will be asked to drink a tasteless liquid which

contains the carbon as part of the substance that the bacteria breaks

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

contain carbon dioxide. This test provides the advantage of being able to

monitor the 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 is especially true in ulcers ofthe greater (large) curvatureof the stomach; most are also a consequence

of chronic H. pyloriinfection.

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.

[edit]Macroscopic appearance

A benign gastric ulcer (from the antrum) of a gastrectomyspecimen.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. In
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the ulcerative form of gastric cancer the borders are irregular. Surrounding

mucosa may present radial folds, as a consequence of the parietal

scarring.

[edit]Microscopic appearanceA 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.[20]

[edit]Differential diagnosis of epigastric pain Peptic ulcer

Gastritis Stomach cancer

Gastroesophageal reflux disease

Pancreatitis

Hepatic congestion

Cholecystitis

Biliary colic

Inferior myocardial infarction

Referred pain (pleurisy, pericarditis)

Superior mesenteric artery syndrome

[edit]TreatmentYounger patients with ulcer-like symptoms are often treated

with antacids or H2 antagonists before EGD is undertaken. Bismuth

compounds may actually reduce or even clear organisms, though the

warning labels of some bismuth subsalicylate products indicate that the

product should not be used by someone with an ulcer.

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may

also be prescribed a prostaglandinanalogue (Misoprostol) in order to help

prevent peptic ulcers, which may be a side-effect of the NSAIDs.

When H. pyloriinfection is present, the most effective treatments are

combinations of 2 antibiotics

(e.g. Clarithromycin, Amoxicillin,Tetracycline, Metronidazole) and 1 proton

pump inhibitor (PPI), sometimes together with a bismuth compound. In
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complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin +

clarithromycin + metronidazole) may be used together with a PPI and

sometimes with bismuth compound. An effective first-line therapy for

uncomplicated cases would

be Amoxicillin + Metronidazole +Pantoprazole (a PPI). In the absenceof H. pylori, long-term higher dose PPIs are often used.

Treatment of H. pyloriusually 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.

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.

[edit]Epidemiology

Disability-adjusted life year for peptic ulcer disease per 100,000 inhabitants in 2004.[21]

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

The lifetime risk for developing a peptic ulcer is approximately 10%.[22]

In Western countries the prevalence of 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. Transmission is by food,contaminated groundwater, and through human saliva (such as from

kissing or sharing food utensils.)[citation needed]

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.
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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. [23] The reason why the

rates of peptic ulcer disease decreased is thought to be the development

of new effective medication and acid suppressants and the discovery ofthe cause of the condition, H. pylori.

In the United States about 4 million people have active peptic ulcers and

about 350,000 new cases are diagnosed each year. Four times as many

duodenal ulcers as gastric ulcers are diagnosed. Approximately 3,000

deaths per year in the United States are due to duodenal ulcer and 3,000

to gastric ulcer. [24]

[edit]History

See also:Timeline of peptic ulcer disease and Helicobacter pyloriJohn 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.[25]

Helicobacter pyloriwas rediscovered in 1982 by

two Australian scientists, Robin Warren and Barry J. Marshall as a

causative factor for ulcers.[26] In their original paper, Warren and Marshall

contended that most stomach ulcers and gastritis were caused by

colonization with this bacterium, not by stress or spicy food as had been

assumed before.[27]

The H. pylorihypothesis was poorly received,[citation needed] 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.[28] This experiment was published in 1984 in the

Australian Medical Journal and is among the most cited articles from thejournal.

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. pyloriand ulcers. This campaign
http://wiki/20th_centuryhttp://wiki/United_Stateshttp://w/index.php%3Ftitle=Peptic_ulcer&action=edit&section=12http://wiki/Timeline_of_peptic_ulcer_disease_and_Helicobacter_pylorihttp://wiki/John_Lykoudishttp://wiki/General_practitionerhttp://wiki/Greecehttp://wiki/Peptic_ulcer_diseasehttp://wiki/Peptic_ulcer_diseasehttp://wiki/Antibioticshttp://wiki/Bacteriahttp://wiki/Helicobacter_pylorihttp://wiki/Australiahttp://wiki/Robin_Warrenhttp://wiki/Barry_Marshallhttp://wiki/Stress_(medicine)http://wiki/Spicy_foodhttp://wiki/Helicobacter_pylorihttp://wiki/Wikipedia:Citation_neededhttp://wiki/Wikipedia:Citation_neededhttp://wiki/Wikipedia:Citation_neededhttp://wiki/Petri_dishhttp://wiki/Halitosishttp://wiki/Centers_for_Disease_Control_and_Preventionhttp://wiki/H._pylorihttp://wiki/20th_centuryhttp://wiki/United_Stateshttp://w/index.php%3Ftitle=Peptic_ulcer&action=edit&section=12http://wiki/Timeline_of_peptic_ulcer_disease_and_Helicobacter_pylorihttp://wiki/John_Lykoudishttp://wiki/General_practitionerhttp://wiki/Greecehttp://wiki/Peptic_ulcer_diseasehttp://wiki/Peptic_ulcer_diseasehttp://wiki/Antibioticshttp://wiki/Bacteriahttp://wiki/Helicobacter_pylorihttp://wiki/Australiahttp://wiki/Robin_Warrenhttp://wiki/Barry_Marshallhttp://wiki/Stress_(medicine)http://wiki/Spicy_foodhttp://wiki/Helicobacter_pylorihttp://wiki/Wikipedia:Citation_neededhttp://wiki/Petri_dishhttp://wiki/Halitosishttp://wiki/Centers_for_Disease_Control_and_Preventionhttp://wiki/H._pylori


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reinforced the news that ulcers are a curable infection, and that health can

be greatly improved and money saved by disseminating information

about H. pylori.[29]

In 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 pyloriand its role

in gastritis and peptic ulcer disease". Professor Marshall continues

research related to H. pyloriand runs a molecular biology lab at UWA in

Perth, Western Australia.

It was a previously widely accepted misunderstanding that the use of

chewing gum resulted in gastric ulcers. The medical profession believed

that this was because the action of masticating on gum caused the over-

stimulation of the production of hydrochloric acid in the stomach. The low

(acidic) pH (pH 2), or hyperchlorhydria was then believed to cause erosion

of the stomach lining in the absence of food, thus causing the development

of the gastric ulcers.[30]

On the other hand, in the recent past, some believed that natural tree resin

extract, mastic gum, actively eliminates the H. pyloribacteria.[31] However,

multiple subsequent studies have found no effect of using mastic gum on

reducing H. pylorilevels.[32][33]

[edit]Notes1. ^ 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)

2. ^ Sonnenberg in his study cautiously

concludes that, among other potential factors

that were found to correlate to ulcer healing,

"moderate alcohol intake might [also] favorulcer healing" (p. 1066)

[edit]References1. ^ ab"GI Consult: Perforated Peptic Ulcer".

Retrieved 2007-08-26.

2. ^ "Peptic Ulcer". Retrieved 2010/06/18.
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3. ^ "Peptic ulcer". Retrieved 2010/06/18.

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Helicobacter pylori, and Smoking". Journal of

Clinical Gastroenterology24 (1): 217. PMID

9013343.PMID9013343. Retrieved 2010-03-18.

13.^ 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. National Digestive Diseases

Information Clearinghouse

14.^ A, Sonnenberg; Mller-Lissner SA, Vogel E,

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16.^ Wachirawat W, Hanucharurnkul S,

Suriyawongpaisal P, et al. (2003). "Stress, but not

Helicobacter pylori, is associated with peptic ulcer

disease in a Thai population". J Med Assoc

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31.^ Huwez FU, Thirlwell D, Cockayne A, Ala'Aldeen

DA (December 1998). "Mastic gum kills

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2003). "Monotherapy with mastic does not

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71. doi:10.1093/jac/dkg057. PMID12562704.

33.^ Bebb JR, Bailey-Flitter N, Ala'Aldeen D, Atherton

JC (September 2003). "Mastic gum has no effect

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3. doi:10.1093/jac/dkg366. PMID12888582.

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