Peptic Ulcer1

8/3/2019 Peptic Ulcer1

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ULCERS, PEPTIC (GASTRIC, DUODENAL)- A circumscribed excavation of the gastric or duodenal mucosal wall that penetratesthe muscularis mucosae and exposes it to acid and pepsin.Causes and Incidence The precise etiologic mechanisms of peptic ulcer formation are unclear.However, recent research points to infection by Helicobacter pylori bacteria as the major factor inulcer formation. Other factors that have been implicated include use of certain drugs (e.g., aspirinand other nonsteroidal antiinflammatory agents ([NSAIDs]); use of alcohol, cigarettes, andcaffeine; and a familial history of ulcers. Those at risk of a duodenal ulcer have increased acidproduction and type O blood. Risk factors for a gastric ulcer include type A blood and underlyingdisease processes such as pancreatitis, gastritis, and hepatic disorders. About 80%of all pepticulcers are duodenal in origin, and the remain-ing 20% are gastric. Gastric ulcers strike men and

women equally, with the peak incidence occurring between ages 55 and 65. There are 40,000 to80,000 cases reported annually in the United States. Duodenal ulcers occur in men two to threetimes as often as in women, and the incidence increases with age. The annual incidence is 200,000to 300,000, but it has been steadily decreasing since the 1950s.Disease Process The pathology is unclear, but it is hypothesized that H. pylori or other factorsmay upset the balance between ulcer-promoting factors, such as secretion of acid and pepsin andfactors that serve as protectors of the mucosal lining, such as mucus production and replacement of

damaged mucosal cells. This sets up an inflammatory process, with resultant ulceration,thrombosis, fibrosis, and scarring of the muscularis mucosae layer of the stomach or duodenum.Symptoms Manifestations vary with location, and ulcers are often asymptomatic or associated

with vague symptoms. Only about 50% of individuals have a characteristic pattern of symptoms.The characteristic pain is described as burning, gnawing, or aching and is located in a well-circumscribed epigastric area. In duodenal ulcers the pain usually appears midmorning, is relieved

by food, and then reappears 2 to 3 hours after eating. It also wakens the individual 2 to 3 hoursafter falling asleep. It occurs daily for 1 week or longer and may then disappear without treatment.

With a gastric ulcer the pain usually occurs after eating food, is located in the left midgastric area,and often radiates to the back. Epigastric pain occurs with an empty stomach. Pain in bothinstances is typically relieved by antacids or milk.Potential Complications Complications include hemorrhage and perforation of the stomach orduodenum, with resulting peritonitis and obstruction of the pylorus or gastric outlet.

Diagnostic TestsEndoscopy/biopsyTo establish presence of ulcer and determine whether malignancy is presentUpper gastrointestinal seriesMay reveal ulcers overlooked on endoscopyGastric analysisIncreased output with duodenal ulcer; decreased or normal output with gastric ulcerCarbon 13 urea breath testLow levels of 13C in exhaled breath indicative of H. pylori infectionTreatmentsSurgeryGastrectomy, gastroduodenostomy, gastrojejunostomy to remove gastrin-producing portion ofstomach in intractable cases with complications; fundic vagotomy with chronic duodenal ulcer

disease.DrugsHistamine receptor antagonists to block gastric acid output; antacids to reduce pain;cytoprotectives (Sucralfate) to form a protective coating in the base of the ulcer; bismuthpreparations in combination with antiinfective drugs for H. pylori (not yet approved in the UnitedStates); omeprazole is a proton pump inhibitor in clinical trials in the United States; prostaglandinsare in clinical trials for treatment associated with NSAID use.
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GeneralAvoidance of alcohol and tobacco products; avoidance of pepper, coffee (caffeinated anddecaffeinated), and foods that cause epigastric distress; avoidance of NSAIDs.

http://www.medi-info.com/ulcers-peptic-gastric-duodenal/

A peptic ulcer, also known as PUD orpeptic ulcer disease,[1]is the most common ulcer of an area of

the gastrointestinal tractthat is usually acidic and thus extremely painful. It is defined as mucosal erosions

equal to or greater than 0.5 cm. As many as 7090% of such ulcers are associated withHelicobacter

pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach; however, only 40%

of those cases go to a doctor. Ulcers can also be caused or worsened by drugs such

asaspirin,Plavix (clopidogrel),ibuprofen, and otherNSAIDs.

Contrary to general belief, four times as many peptic ulcers arise in the duodenumthe first part of

the small intestine, just after the stomachrather than in thestomachitself. About 4% of stomach ulcers

are caused by a malignanttumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are

generallybenign.

Classification

By Region/Location

Duodenum (called duodenal ulcer)

Oesophagus (called esophageal ulcer)

Stomach (called gastric ulcer)

Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)

Modified Johnson Classification of peptic ulcers:

Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura

angularis along the locus minoris resistentiae.

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 ulcer

Type V: Can occur throughout the stomach. Associated with chronic NSAID use (such as aspirin).
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Signs and symptoms

Symptoms of a peptic ulcer can be

abdominal pain, classically epigastric with severity relating to mealtimes, after around three hours

of taking 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 -

although this is more associated withgastroesophageal 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 oxidizediron fromhemoglobin);

rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This

is extremely painful and requires immediate surgery.

A history ofheartburn, 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

mostglucocorticoids(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 esophagogastroduodenoscopy.

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers:

A gastric ulcer would giveepigastricpain during the meal, asgastric acidproduction is increased as food

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

sphinctercloses to concentrate the stomach contents, therefore acid is not reaching the duodenum.

Duodenal ulcer pain would manifest mostly 23 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.

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,childrenand theelderlydo not develop any symptoms

unless complications have arisen.
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Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly

accompanies ulcers. This pain can be misinterpreted ashunger, indigestionorheartburn. Pain is usually

caused by the ulcer but it may be aggravated by the stomach acidwhen 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 flare at night and it can commonly be temporarily relieved 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 common complication. Sudden large bleeding can be life-

threatening.[5]It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal

artery.

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 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 intense abdominal pain. Posterior wall perforation

leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of

duodenum.

Penetration is when the ulcer continues into adjacent organs such as the liver andpancreas.[6]

Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet

obstruction. Patient often presents with severe vomiting.

Canceris included in the differential diagnosis (elucidated by biopsy), Helicobacter pylorias the

etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.[7]

Cause

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronicinflammationdue

to Helicobacter pylorithat colonizesthe antralmucosa[citation needed]. The immune system is unable to clear

the infection, despite the appearance of antibodies. Thus, thebacteriumcan cause a chronic

active gastritis(type B gastritis), resulting in a defect in the regulation ofgastrinproduction by that part of

the stomach, and gastrin secretion can either be increased, or as in most cases, decreased, resulting in

hypo- orachlorhydria.Gastrinstimulates the production ofgastric acidby parietal cells and, in H.

pyloricolonization responses that increase gastrin, the increase in acid can contribute to the erosion of

the mucosa and therefore ulcer formation.
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Another major cause is the use ofNSAIDs(see above). The gastric mucosa protects itself from gastric

acidwith a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block

the function ofcyclooxygenase1 (cox-1), which is essential for the production of these prostaglandins.

COX-2 selective anti-inflammatories (such as celecoxib or 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 ofH. 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 among

individuals 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 ofH. 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

asdiet,spiceconsumption 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 that alcohol 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 atstress as a possible cause, or at least complication, 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.

An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are

not purely aninfectious 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 stress has 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]
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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.[16]

Diagnosis

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

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, this indicating that their primary diagnosis was

accurate.

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrastx-

rays. The tests are typically ordered if 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,

becausestomach cancercan 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 may suspect an

underlying condition that causes the stomach to overproduceacid.[2]

An esophagogastroduodenoscopy(EGD), a form ofendoscopy, 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.

One of the reasons that blood tests are not reliable for 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 result is possible with a blood test if the patient has recently been taking certain drugs,

such as antibiotics orproton pump inhibitors.[17]
http://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-17http://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-17http://en.wikipedia.org/wiki/Gastric_cancerhttp://en.wikipedia.org/wiki/Gastric_cancerhttp://en.wikipedia.org/wiki/Gastric_cancerhttp://en.wikipedia.org/wiki/X-rayshttp://en.wikipedia.org/wiki/X-rayshttp://en.wikipedia.org/wiki/X-rayshttp://en.wikipedia.org/wiki/Weight_losshttp://en.wikipedia.org/wiki/Weight_losshttp://en.wikipedia.org/wiki/Stomach_cancerhttp://en.wikipedia.org/wiki/Stomach_cancerhttp://en.wikipedia.org/wiki/Acidhttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-Peptic_Ulcer-1http://en.wikipedia.org/wiki/Esophagogastroduodenoscopyhttp://en.wikipedia.org/wiki/Endoscopyhttp://en.wikipedia.org/wiki/Gastroscopyhttp://en.wikipedia.org/wiki/Blood_testshttp://en.wikipedia.org/wiki/Antibioticshttp://en.wikipedia.org/wiki/Proton_pump_inhibitorshttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-18http://en.wikipedia.org/wiki/File:Gastric_ulcer_3.jpghttp://en.wikipedia.org/wiki/File:Gastric_ulcer_3.jpghttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-17http://en.wikipedia.org/wiki/Gastric_cancerhttp://en.wikipedia.org/wiki/X-rayshttp://en.wikipedia.org/wiki/X-rayshttp://en.wikipedia.org/wiki/Weight_losshttp://en.wikipedia.org/wiki/Stomach_cancerhttp://en.wikipedia.org/wiki/Acidhttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-Peptic_Ulcer-1http://en.wikipedia.org/wiki/Esophagogastroduodenoscopyhttp://en.wikipedia.org/wiki/Endoscopyhttp://en.wikipedia.org/wiki/Gastroscopyhttp://en.wikipedia.org/wiki/Blood_testshttp://en.wikipedia.org/wiki/Antibioticshttp://en.wikipedia.org/wiki/Proton_pump_inhibitorshttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-18


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The diagnosis ofHelicobacter 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

labs are not set up to perform H. pyloricultures;

Direct detection ofurease activity in a biopsy specimen byrapid urease test;

Measurement ofantibodylevels inblood (does not require EGD). It is still somewhat controversial

whether a positive antibody without EGD is enough to warrant eradication therapy;

Stoolantigentest;

Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon atom to detect H. pylori.[18]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 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 monitor the response to treatment used to kill the bacteria.

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

This is especially true in ulcers of thegreater (large) curvature of 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 theperitoneal 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
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A benign gastric ulcer (from the antrum) of agastrectomy specimen.

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 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 appearance

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.[19]

[edit]Differential diagnosis

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

Treatment

Younger patients with ulcer-like symptoms are often treated with antacids orH2 antagonistsbefore EGD

is undertaken.Bismuth compoundsmay actually reduce or even clear organisms[citation needed], though the

warning labels of some bismuth subsalicylate products indicate that the product should not be used by

someone with an ulcer.[20]
http://en.wikipedia.org/wiki/Gastrectomyhttp://en.wikipedia.org/wiki/Gastrectomyhttp://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=8http://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=8http://en.wikipedia.org/wiki/Muscularis_mucosaehttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-pathologyatlas-20http://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-pathologyatlas-20http://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=9http://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=9http://en.wikipedia.org/wiki/Gastritishttp://en.wikipedia.org/wiki/Stomach_cancerhttp://en.wikipedia.org/wiki/Gastroesophageal_reflux_diseasehttp://en.wikipedia.org/wiki/Pancreatitishttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Congestionhttp://en.wikipedia.org/wiki/Cholecystitishttp://en.wikipedia.org/wiki/Biliary_colichttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Referred_painhttp://en.wikipedia.org/wiki/Pleurisyhttp://en.wikipedia.org/wiki/Pleurisyhttp://en.wikipedia.org/wiki/Pericarditishttp://en.wikipedia.org/wiki/Superior_mesenteric_artery_syndromehttp://en.wikipedia.org/wiki/Antacidhttp://en.wikipedia.org/wiki/H2_antagonisthttp://en.wikipedia.org/wiki/H2_antagonisthttp://en.wikipedia.org/wiki/H2_antagonisthttp://en.wikipedia.org/wiki/Bismuth_subsalicylatehttp://en.wikipedia.org/wiki/Bismuth_subsalicylatehttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-PEPTO-21http://en.wikipedia.org/wiki/File:Benign_gastric_ulcer_1.jpghttp://en.wikipedia.org/wiki/Gastrectomyhttp://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=8http://en.wikipedia.org/wiki/Muscularis_mucosaehttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-pathologyatlas-20http://en.wikipedia.org/w/index.php?title=Peptic_ulcer&action=edit&section=9http://en.wikipedia.org/wiki/Gastritishttp://en.wikipedia.org/wiki/Stomach_cancerhttp://en.wikipedia.org/wiki/Gastroesophageal_reflux_diseasehttp://en.wikipedia.org/wiki/Pancreatitishttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Congestionhttp://en.wikipedia.org/wiki/Cholecystitishttp://en.wikipedia.org/wiki/Biliary_colichttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Referred_painhttp://en.wikipedia.org/wiki/Pleurisyhttp://en.wikipedia.org/wiki/Pericarditishttp://en.wikipedia.org/wiki/Superior_mesenteric_artery_syndromehttp://en.wikipedia.org/wiki/Antacidhttp://en.wikipedia.org/wiki/H2_antagonisthttp://en.wikipedia.org/wiki/Bismuth_subsalicylatehttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Peptic_ulcer#cite_note-PEPTO-21


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

aprostaglandinanalogue(Misoprostol) in order to help prevent peptic ulcers, which may be a side-

effectof the NSAIDs.

When H. pyloriinfection is present, the most effective treatments are combinations of 2 antibiotics

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

sometimes together 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. An effective first-line therapy for uncomplicated cases would

be Amoxicillin +Metronidazole+ Pantoprazole(a PPI). In the absence ofH. pylori, long-term higher dose

PPIs are often used.

Treatment ofH. 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, orclipping.

Ranitidineprovides relief of peptic ulcers, heartburn, indigestion and excess stomach acid and prevention

of these symptoms associated with excessive consumption of food and drink. Ranitidine is available over

the counter from a pharmacy and works by decreasing the amount of acid the stomach produces allowing

healing of ulcers. Zantac tablets contain Ranitidine 150 mg as the active ingredient which can also be

bought generically.[21]

Sucralfate, (Carafate) has also been a successful treatment of peptic ulcers.[22]

[edit]Epidemiology

Disability-adjusted life yearfor peptic ulcer disease per 100,000 inhabitants in 2004.[23]

no data

less than 20
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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%.[24]

In Western countries the prevalence ofHelicobacter pyloriinfections 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).[25]

A minority of cases ofH. pyloriinfection will eventually lead to an ulcer and a larger proportion of people

will 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. [26]The reason

that the 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.

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.[27]

[edit]History

See also:Timeline of peptic ulcer disease and Helicobacter pylori
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John Lykoudis, a general practitionerin Greece, treated patients forpeptic ulcer diseasewith antibiotics,

beginning in 1958, long before it was commonly recognized that bacteria were a dominant cause for the

disease.[28]

Helicobacter pyloriwas rediscovered in 1982 by two Australianscientists, Robin Warren and Barry J.

Marshall as a causative factor for ulcers.[29]In their original paper, Warren and Marshall contended that

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

foodas had been assumed before.[30]

The H. pylorihypothesis was poorly received,[31]so in an act of self-experimentation Marshall drank

aPetri dish containing a culture of organisms extracted from a patient and five days later developed

gastritis. His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria

at the urging of his wife, sincehalitosis is one of the symptoms of infection.[32]This experiment was

published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal.

In 1997, theCenters 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 betweenH. pyloriand 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 about H. pylori.[33]

In 2005, theKarolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicineto Dr.

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

pyloriand its role in gastritisand peptic ulcer disease." Professor Marshall continues research related

to H. pyloriand runs a molecular biology lab atUWA in Perth, Western Australia.

Some believed thatmastic gum, a tree resin extract, actively eliminates the H. pyloribacteria.[34]However,

multiple subsequent studies have found no effect of using mastic gum on reducing H. pylorilevels.[35][36]

http://en.wikipedia.org/wiki/Peptic_ulcer

Peptic UlcerPosted by: Lhynnelli, RN

Is a lesion in the mucosa of the lower esophagus, stomach, pylorus, or duodenum.

also known as ulcus pepticum, PUD orpeptic ulcer disease, is an ulcer (defined as mucosal erosions

equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely

painful
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Causative factors include mucosal infection by the bacterium Helicobacter pylori (mechanism unclear).

Use of non-steroidal anti-inflammatory drugs (NSAIDs), especially aspirin.

Genetic factors such as cigarette smoking, stress, and lower socio-economic status may play a role.

Complications include GI hemorrhage, perforation, and gastric outlet obstruction.

Classification

Stomach (called gastric ulcer)

Duodenum (called duodenal ulcer)

Oesophagus (called Oesophageal ulcer)

Meckels Diverticulum (called Meckels Diverticulum ulcer)

Types of peptic ulcers

Type I: Ulcer along the lesser curve of stomach

Type II: Two ulcers present one gastric, one duodenal

Type III: Prepyloric ulcer

Type IV: Proximal gastroesophageal ulcer

Type V: Anywhere along gastric body, NSAID induced

Assessment

1. Abdominal pain

Occurs in the epigastric area radiating to the back; described as dull, aching, and gnawing.

Pain may increase when the stomach is empty, at night, or approximately 1 to 3 hours after eating.

Pain is relieved by taking antacids (common with duodenal ulcers).

2. Nausea, anorexia, early satiety (common with gastric ulcers), belching.

3. Dizziness, syncope, hematemesis, melena with GI hemorrhage:

Positive fecal occult blood

Decreased hemoglobin and hematocrit, indicating anemia.

Orthostatic blood pressure and pulse changes.

4. Peptic ulcer disease may be asymptomatic in up to 50% of persons affected5. Differentiating Gastric and Duodenal Ulcers:

Gastric Ulcer Duodenal Ulcer

Gnawing epigastric painoccurring 30 minutes to 1

hour after meals

Gnawing epigastric painoccurring 2-3 hours after meals

Aggravated by eating Relieved by food (because the


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(because acid secretion

increase at meal time) leads to

weight loss

pyloric sphincter, at the

junction of stomach and

duodenum, closes upon eating

to concentrate food in thestomach) causes weight gain

Relieved by vomiting

(because acid is expelled out)

Not relived

No pain at hours of sleep

(HCl production decreases athours of sleep)

Pain at hours of sleep (because

gastric emptying continuous athours of sleep)

More common in persons

older than age 50

More common between ages

25 and 50

6.

7.

DiagnosticEvaluation

1. Upper GI series usually outlines ulcer or area of inflammation.

2. Endoscopy (esophagogastroduodenoscopy) visualizes duodenal mucosa and helps identify inflammatory

changes, lesions, bleeding sites, and malignancy (through biopsy and cytology).

3. Gastric secretory studies ( gastric acid secretion test, serum gastrin level tst) are elevated in Zollinger-

Ellison syndrome.

4. H. pylori antibody titer may be positive, especially in recurrent ulcers; however, there is high rate of false

positive results; C-urea breath test or biopsy testing is more definitive test for H. pylori.

Pharmacologic Interventions

1. Histamine2 (H2) receptor antagonists such as ranitidine to reduce gastric acid secretions.

2. Antisecretory or proton-pump inhibitor, such as omeprazole, to help ulcer heal quickly in 4 to 8 hours.

3. Cytoprotective drug sucralfate, which protects ulcer surface against acid, bile, and pepsin.

4. Antacids to reduce acid concentration and help reduce symptoms.

5. Anti-biotic as part of a multi-drug regimen to eliminate H. pylori to prevent reoccurrence.

Surgical Interventions

Surgery is indicated for hemorrhage, perforation, obstruction, and when unresponsive to medical therapy. Procedures

include:
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1. Gastroduodenostomy (Billroth I)

Partial gastrectomy with removal of antrum and pylorus; gastric stump is anastomosed to

duodenum.

2. Gastrojejunostomy (Billroth II)

Partial gastrectomy with removal of antrum and pylorus; gastric stump is anastomosed to jejunum.

3. Antrectomy Antrum (lower half of stomach), pylorus and small cuff of duodenum are resected; stomach is

anastomosed to jejunum and duodenal stump is closed.

4. Total gastrectomy

Removal of stomach with anastomosis of esophagus to jejunum or duodenum.

5. Pyloroplasty

Longitudinal incision is made in the pylorus, and closed transversely to permit the muscle to relax

and established an enlarged outlet; often performed with vagotomy.

Nursing Interventions

1. Monitor the patient for signs of bleeding through fecal occult blood, vomiting, persistent diarrhea, and

change in vital signs.

2. Monitor intake and output.

3. Monitor the patients hemoglobin, hematocrit, and electrolyte levels.

4. Administered prescribed I.V. fluids and blood replacements if acute bleeding is present.

5. Maintain nasogastric tube for acute bleeding, perforation, and postoperatively, monitor tube drainage for

amount and color.

6. Perform saline lavage if ordered for acute bleeding.

7. Encourage bed rest to reduce stimulation that may enhance gastric secretion.

8. Provide small, frequent meals to prevent gastric distention if not actively bleeding.

9. Watch for diarrhea caused by antacids and other medications.

10. Restrict foods and fluids that promote diarrhea and encourage good perineal care.

11. Advise patient to avoid extremely hot or cold food and fluids, to chew thoroughly, and to eat in a leisurely

fashion to reduce pain.

12. Administer medications properly and teach patient dose and duration of each medication.13. Advise patient to modify lifestyle to include health practices that will prevent recurrences of ulcer pain and

bleeding.

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Peptic Ulcer1