Peptic Ulcermazher

8/3/2019 Peptic Ulcermazher

1/49

1

TOPIC= PEPTIC ULCER

SUBMITTED TO SYED NASIR ASGHAR


2/49

2

Peptic ulcer

Definition of ulcer: A lesion of the skin or a mucousmembrane such as the one lining the stomach or

duodenum that is accompanied by formation of pus

and necrosis of surrounding tissue, usually resulting

from inflammation or ischemia.

Ulcer: An area of tissue erosion, for example, of the skin

or lining of the gastrointestinal (GI) tract. Due to theerosion, an ulcer is concave. It is always depressed below

the level of the surrounding tissue.

Ulcers can have diverse causes. Ulcers on the skin are

often due to irritation, as with bedsores, and they may

become infected and inflamed as they grow.

Ulcers in the GI tract were once attributed to stress butmost are now believed to be due to infection with the

. GI ulcers, however, may be madeH. pyloridusbacteria

and other noninfectious factors.smokingworse by stress,

The word "ulcer" traveled across the English Channel

from the French "ulcere" which, in turn, came from the

Latin "ulcus, ulceris" meaning "sore, sore spot, painful

spot, or ulcer."


3/49

3

1-Definition:

A peptic ulcer, also known as PUD or peptic ulcer disease, is an

ulcer (defined as mucosal erosions equal to or greater than 0.5

that is usually acidicgastrointestinal tractcm) of an area of theand thus extremely painful.

Peptic ulcers are open sores that develop on the inside lining of

your esophagus, stomach and the upper portion of your small

intestine. The most common symptom of a peptic ulcer is

abdominal pain.

Peptic ulcers that occur on the inside of the stomach are called

gastric ulcers. Peptic ulcers that occur inside the hollow tube

(esophagus) where food travels from your throat to your stomach

are called esophageal ulcers. Peptic ulcers that affect the inside of

the upper portion of your small intestine (duodenum) are called

duodenal ulcers.


4/49

4

&a peptic ulcer is an area of damage to the lining of either thestomach or the wall of the small bowel. &Ulcers are defined as a breach in the mucosa of the alimentary

tract, which extends through the muscularis mucosa into the sub

mucosa or deeper.

(Erosion differs from an ulcer in being partial thickness mucosaldefect).

&Peptic ulcers are chronic most often solitary, lesions that occur

in any portion of gastrointestinal tract exposed to the aggressive

action of acid-peptic juices.

Causes:

Eenvironmental and hereditary factors influencecommon medical diseases including peptic ulceralthough Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAID) use are main aetiologicalfactors for peptic ulcer (liu et al, 2009.

1.Helicobacter pyloriIt is a helical (spiral) shaped microaerophilic gram-negative bacillus. It has four to six sheathed flagella.The organism is slowly growing in vitro and grows onblood agar and selective blood agar medium(Skirrows) (Malaty, 2007). The organism produces


5/49

5

urease and mucolytic proteases that are important forits survival and pathogenic effect. The organismsvirulence factors needed for colonization includesmotility, adhesins, proteases, phospholipases, cytokines,

cytotoxins and urease. Urease most likely protects theorganism from the acidic environment (Sedlack andViggiano, 2008).

2.NSAID (Non-steroidal anti-inflammatorydrugs)

NSAID use is a common cause of peptic ulcer disease.Within14 days after the start of such treatment, about5% of patients develop gastric mucosal erosions or ulcers.If usage continues for4 weeks or longer, this proportionincreases to10%. The risk of developing ulcer with NASIDuse is higher in older patients, patients with a previoushistory of ulcer and in patients who use corticosteroids(Kuipers and Blaser, 2007).

3.Environmental factors (smoking, stress anddiet)

Duggan and Duggan (2006) suggested a link betweensmoking and peptic ulcer disease. About diet, theyperceived little evidence in the literature correlatingalcohol, caffeine and fibre intake to peptic ulcer disease.They suggested high sugar intake correlates toduodenal ulcer, while high salt intake links toincreased gastric ulcer risk. Stress influences duodenalulcers more than gastric ulcer (Szabo et al, 2007).

4.Genetic considerationsDuggan and Duggan (2007) suggested that 39% to 62%

of susceptibility to peptic ulcer disease is explainable on

hereditary basis. They suggested heredity is determining

to the acquisition of Helicobacter pylori, with no link


6/49

6

between genetic factors responsible for developing peptic

ulcer and those responsible for Helicobacter acquisition

Peptic ulcers occur when acid in the digestive tract eats

away at the inner surface of the esophagus, stomach orsmall intestine. The acid can create a painful open sorethat may bleed.

Digestive tract is coated with a mucous layer thatnormally protects against acid. But if the amount ofacid is increased or the amount of mucus is decreased,you could develop an ulcer. Causes include:

y A bacterium. A common cause of ulcers is thecorkscrew-shaped bacterium Helicobacter pylori. H.pylori bacteria commonly live and multiply within themucous layer that covers and protects tissues that linethe stomach and small intestine. Often, H. pylori causesno problems. But sometimes it can disrupt the mucouslayer and inflame the lining of your stomach orduodenum, producing an ulcer. It's not clear how H.

pylori spreads. It may be transmitted from person toperson by close contact, such as kissing. People may alsocontract H. pylori through food and water.

y Regular use of pain relievers. Certain over-the-counterand prescription pain medications can irritate orinflame the lining of your stomach and small intestine.These medications include aspirin, ibuprofen (Advil,Motrin, others), naproxen (Aleve, Anaprox, others),

ketoprofen and others. Peptic ulcers are more commonin older adults who take pain medications frequently,such as might be common in people with osteoarthritis.To help avoid digestive upset, take pain relievers withmeals. If you have been diagnosed with an ulcer, makesure your doctor knows this when prescribing any pain


7/49

7

reliever. The pain reliever acetaminophen (Tylenol,others) doesn't cause peptic ulcers.

y Other medications. Other prescription medications that

can also lead to ulcers include medications used totreat osteoporosis called bisphosphonates (Actonel,Fosamax, others).

The lining of the stomach is usually protected from thedamaging effects of stomach acid. When that protectionfails, an ulcer forms. There are a few different ways thishappens.

y Helicobacter pylori (H. pylori)--H. pylori, a type ofbacteria, is responsible for most ulcers. Thisorganism weakens the protective coating of thestomach and first part of the intestine and allowsdamaging digestive juices to eat away at thesensitive lining below. As many as 20% of Americansover age40 have H. pylori living in their digestivetract, but most do not develop ulcers.

y Nonsteroidal anti-inflammatory drugs (NSAIDs) Long-term use of these pain relievers is the secondmost common cause of ulcers. These drugs blockprostaglandins, substances in the stomach that helpmaintain blood flow and protect the area frominjury. Some people are more susceptible to this side


8/49

8

effect of NSAIDs than others. These drugs includeibuprofen (Advil, Motrin), naproxen (Aleve), andketoprofen (OrudisKT), as well as prescription drugs.Some may be more likely to produce ulcers than

others. If you must use long-term pain medications,talk to your doctor about which ones are safest.

Other causes of ulcers are conditions that can result indirect damage to the wall of the stomach or duodenum,such as heavy use of alcohol, radiation therapy, burns,and physical injury.

A major causative factor (60% of gastric and up to 90%

of duodenal ulcers) is chronic inflammation due toHelicobacter pylori that colonizes the antralmucosa. Theimmune system is unable to clear the infection, despitethe appearance of antibodies. Thus, the bacterium cancause a chronic active gastritis (type B gastritis),resulting in a defect in the regulation of gastrinproduction by that part of the stomach, and gastrinsecretion can either be decreased (most cases) resulting

in hypo-or achlorhydria or increased. Gastrinstimulates the production of gastric acid by parietalcells and, in H. pylori colonization responses thatincrease gastrin, the increase in acid can contribute tothe erosion of the mucosa and therefore ulcer formation.

Another major cause is the use of NSAIDs The gastricmucosa protects itself from gastric acid with a layer ofmucus, the secretion of which is stimulated by certain

prostaglandins. NSAIDs block the function ofcyclooxygenase1 (cox-1), which is essential for theproduction of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the sincewithdrawn rofecoxib) preferentially inhibit cox-2, whichis less essential in the gastric mucosa, and roughly halve


9/49

9

the risk of NSAID-related gastric ulceration. As theprevalence of H. pylori-caused ulceration declines in theWestern world due to increased medical treatment, agreater proportion of ulcers will be due to increasing

NSAID use among individuals with pain syndromes aswell as the growth of aging populations that developarthritis.

The incidence of duodenal ulcers has droppedsignificantly during the last 30 years, while theincidence of gastric ulcers has shown a small increase,mainly caused by the widespread use of NSAIDs. The dropin incidence is considered to be a cohort-phenomenonindependent of the progress in treatment of the disease.The cohort-phenomenon is probably explained byimproved standards of living which has lowered theincidence of H. pylori infections.

Although some studies have found correlations betweensmoking and ulcer formation,[9] others have been morespecific in exploring the risks involved and have found

that smoking by itself may not be much of a risk factorunless associated with H. pylori infection Some suggestedrisk factors such as diet, spice consumption and bloodtype, were hypothesized as ulcerogens (helping causeulcers) until late in the 20th century, but have beenshown to be of relatively minor importance in thedevelopment of peptic ulcers. Similarly, while studieshave found that alcohol consumption increases riskwhen associated with H. pylori infection, it does notseem to independently increase risk, and even whencoupled with H. pylori infection, the increase is modestin comparison to the primary risk factor.


10/49

10

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

Stress

Researchers also continue to look at stress as a possiblecause, or at least complication, in the development ofulcers. There is debate as to whether psychological stresscan influence the development of peptic ulcers. Burnsand head trauma, however, can lead to physiologicstress ulcers, which are reported in many patients whoare on mechanical ventilation.

classificationy Stomach (called gastric ulcer)y Duodenum (called duodenal ulcer)y Oesophagus (called Oesophageal ulcer)y Meckels Diverticulum (called Meckels Diverticulum

ulcer)

Types of peptic ulcersy Type I: Ulcer along the lesser curve of stomachy Type II: Two ulcers present one gastric, one

duodenaly Type III: Prepyloric ulcery Type IV: Proximal gastroesophageal ulcery Type V: Anywhere along gastric body, NSAID

induced

Assessment1.Abdominal pain

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

o Pain may increase when the stomach is empty,at night, or approximately1 to 3 hours after


11/49

11

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

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

3.Dizziness, syncope, hematemesis, melena with GIhemorrhage:

o Positive fecal occult bloodo Decreased hemoglobin and hematocrit,

indicating anemia.o Orthostatic blood pressure and pulse changes.

4.Peptic ulcer disease may be asymptomatic in up to50% of persons affecte

Differentiating Gastric and Duodenal Ulcers:

Gastric Ulcer Duodenal Ulcer

Gnawing epigastricpain occurring 30minutes to1 hour after

meals

Gnawing epigastric painoccurring 2-3 hours aftermeals

Aggravated by eating(because acid secretionincrease at meal time)leads to weight loss

Relieved by food(because the pyloricsphincter, at the junctionof stomach andduodenum, closes uponeating to concentratefood in the stomach)

causes weight gainRelieved by vomiting(because acid isexpelled out)

Not relived

No pain at hours ofsleep (HCl production

Pain at hours of sleep(because gastric


12/49

12

decreases at hours ofsleep)

emptying continuous athours of sleep)

More common in

persons older than age50

More common between

ages 25 and 50

Risk factors:You may have an increased risk of peptic ulcers if you:

y Smoke. Smoking may increase the risk of peptic ulcers inpeople who are infected with H. pylori.

y Drink alcohol. Alcohol can irritate and erode themucous lining of your stomach, and it increases the

amount of stomach acid that's produced.

y Have uncontrolled stress. Although stress alone isn't acause of peptic ulcers, it's a contributing factor. You mayundergo stress for a number of reasons an

emotionally disturbing circumstance or event, surgery,

or a physical trauma, such as a burn or other severe

injury


13/49

13

y Heredityy Older agey Chronic pain, from any cause such as arthritis,

fibromyalgia, repetitive stress injuries (like carpaltunnel syndrome), or persistent back pain, causing

long-term use of aspirin or NSAIDs

y Alcohol abusey Diabetes may increase your risk of having H. pyloriy Lifestyle factors, including chronic stress, coffee

drinking (even decaf), and smoking, may make you

more susceptible to damage from NSAIDs or H. pylori if

you are a carrier of this organism. But these factors

do not cause an ulcer on their own.

Signs& symptoms:

Pain is the most common symptom

Burning pain is the most common peptic ulcer symptom.

The pain is caused by the ulcer and is aggravated bystomach acid coming in contact with the ulceratedarea. The pain typically may:

y Be felt anywhere from your navel up to your breastboney Be worse when your stomach is emptyy Flare at nighty Often be temporarily relieved by eating certain foods

that buffer stomach acid or by taking an acid-reducingmedication

y Disappear and then return for a few days or weeks


14/49

14

Other signs and symptomsLess often, ulcers may cause severe signs or symptomssuch as:

y The vomiting of blood which may appear red or blacky Dark blood in stools or stools that are black or tarryy Nausea or vomitingy Unexplained weight lossy Appetite changes

When to see a doctor

See your doctor if you have persistent signs andsymptoms that worry you. Over-the-counter antacidsand acid blockers may relieve the gnawing pain, but therelief is short-lived. If your pain persists, see your doctor.

y Pain may be relieved by antacids or milky Heartburny

Indigestion (dyspepsia)y Belchingy abdominal pain, classically epigastric with severity

relating to mealtimes, after around 3 hours oftaking a meal (duodenal ulcers are classicallyrelieved by food, while gastric ulcers areexacerbated by it);

y bloating and abdominal fullness;y waterbrash (rush of saliva after an episode of

regurgitation to dilute the acid in esophagus-although this is more associated with GERD);

y nausea, and copious vomiting;y loss of appetite and weight loss;y hematemesis (vomiting of blood); this can occur

due to bleeding directly from a gastric ulcer, or


15/49

15

from damage to the esophagus fromsevere/continuing vomiting.

y melena (tarry, foul-smelling feces due to oxidizediron from hemoglobin);

y rarely, an ulcer can lead to a gastric or duodenalperforation, which leads to acute peritonitis. This isextremely painful and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease(GERD) and use of certain forms of medication canraise the suspicion for peptic ulcer. Medicines associatedwith peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, andmost glucocorticoids (e.g. dexamethasone andprednisolone).

Clinical investigations:

Tests and diagnosis

In order to detect an ulcer, you may have to undergo

diagnostic tests, such as:

y Tests for H. pylori. Your doctor may recommend tests todetermine whether the bacterium H. pylori is present inyour body. Which type of test you undergo depends onyour situation. H. pylori may be detected in a blood test,a stool test or a breath test. For the breath test, you drinka small glass of clear, tasteless liquid that containsradioactive carbon. H. pylori breaks down the substancein your stomach. Later, you blow into a bag, which is

then sealed. If you're infected with H. pylori, your breathsample will contain the radioactive carbon in the formof carbon dioxide.

y Using a scope to examine your upper digestive system(endoscopy). During endoscopy, your doctor passes ahollow tube equipped with a lens (endoscope) down your


16/49

16

throat and into your esophagus, stomach and smallintestine. Using the endoscope, your doctor looks forulcers. If your doctor detects an ulcer, he or she mayremove small tissue samples (biopsy) for laboratory

examination. A biopsy can also identify the presence ofH. pylori in your stomach lining. Your doctor is morelikely to recommend endoscopy if you are older, havesigns of bleeding, or have experienced recent weight lossor difficulty eating and swallowing.

y X-ray of your upper digestive system. Sometimes called abarium swallow or upper gastrointestinal series, thisseries of X-rays creates images of your esophagus,

stomach and small intestine. During the X-ray, youswallow a white liquid (containing barium) that coatsyour digestive tract and makes an ulcer more visible.

H. pyloritesty As H. pylori is the most common cause of a peptic

ulcer, your GP may test you for the bacterium and,if necessary, prescribe medicines to treat theinfection.

y H. pylori can be detected in a urea breath test. Youwill be asked to swallow a liquid containing asubstance called urea that is broken down by H.pylori to produce water and carbon dioxide. Yourbreath will then be tested using a machine for theamount of carbon dioxide in it. If the carbondioxide is over a certain level, H. pylori is present.

y Alternatively a sample of your blood or your faeceswill be sent to a laboratory to test for H. pylori.Endoscopy

y If you have a suspected peptic ulcer, your GP mayarrange a gastro-intestinal endoscopy (also calleda gastroscopy). Not everyone who has abdominalpain needs one, so your GP may use one of the other


17/49

17

tests first. However, endoscopy is the only way to becertain whether or not you have a peptic ulcer.

y An endoscopy is a procedure that allows a doctor tolook at the inside of your body. The test is done

using a narrow, flexible, tube-like telescopic cameracalled an endoscope that is passed through yourmouth and into your stomach. The procedureusually lasts a few minutes.

y Your doctor will be able to see the lining of yourstomach and can take a sample of your stomachlining at the same time. This sample is either sent toa laboratory and examined under a microscope, or

directly tested for H. pylo.


18/49

18

y Biopsy is necessary to distinguish between benignand malignant ulcers.

y Biopsy should be taken from the ulcer edge, at leastfrom each quadrant.

y Upto10-12 biopsies may be taken to exclude cancer.y Repeat endoscopy may be necessary if biopsies are

negative and there is high index of suspicion.y

laboratory test

Title&Frequency

1. CBC should be repeated in Once in10 case of

abnormalities revealed days

(fortreatmentmonitoring)

2. Blood type Once

3. Rh-factor Once

4. Feces for occult blood Once

5. Urinalysis Once

6. Iron in blood serum Once

7. Reticulocyte count Once

8. Blood sugar Once

9. Histological and cytological Once

evaluation of biopsy

sample if endoscopy

was conducted


19/49

19

10. Urease test Once**This test is performed to detect active infection. Itsspecificity and sensitivity exceed 90%. May be also used

to diagnose successful eradication of Helicobacterpylori.Antibiotics and bismuth medications should bediscontinued at least four weeks before the test.Ranitidin and other histamine receptors blockers shouldbe discontinued at least seven days prior to theprocedure. The test should be conducted no earlier thansix hours after the last meal.This test is not

recommended in case of the prior partial gastrectomyrelated to gastric cancer, prolonged use of proton pumpinhibitors (Omeprasol, etc.) and severe esophagealreflux and prolonged use of

y NSAID irrespective of the fact whether the ulcer hasdeveloped or not.

Pathophysiology:stomach produces acid to help you digest food. Thelining of your stomach and first part of your small bowel(duodenum) have a layer of mucus that protects themfrom the acid. If this protection mechanism doesn't workproperly, the acid can eat into your stomach lining andcause an ulcer.


20/49

20

The different parts of the digestive system

Stomach (gastric) ulcers and small bowel (duodenal)ulcers are collectively known as peptic ulcers. Duodenalulcers are more common.

Stomach ulcers usually affect people between the ages of40 and 80, and duodenal ulcers affect people aged 20 to60. Peptic ulcers are more common in women than men.

The size of peptic ulcers can vary from one millimetre toseveral centimetres across. They look similar to mouthulcers.


21/49

21

III.PATHOPHYSIOLOGY

Many diseases are roaming around the environmentnow a day. Some have evolved from other diseases; someof these evolved from simpler diseases and after theyhave evolved they have become more dangerous and

complicated. One of these diseases is the peptic ulcer.Peptic ulcer or also known as peptic ulcer disease (PUD)is a type of ulcer that occurs in the area of thegastrointestinal tract that is, most of the time acidichence, it is extremely paiful. There are manyclassifications of ulcer depending on the region or thearea of the body where in it is affected. There is thegastric ulcer which is in the stomach area, theduodenal ulcer which is in the duodenum, the

esophageal ulcer found in the esophagus and there isthe Meckel's diverticulum ulcer found in the Meckel'sdiverticulum. The pathophysiology of peptic ulcerdescribes the causes of ulcer, it's evolution as a diseaseand ways to prevent it and eventually treat it. First wemust know how such disease occurs. Since most of the

erosionofmucosal

wall,infection,

chronic

whenacidand

enzymeovercome

thedefense

mechanism of

infection byH.

pylori

regularintakeof

Aspirinand

nonsteroidal

anti-

caffeine,alcohol stress

cigarette

stomach pain,nausea,

vomiting,lossof

appetite,lossof

weight,

severe ulcermay cause

stomach produces

HClandanenzyme

calledpepsin to

digest food

vomiting of

bloodordark

materials, black


22/49

22

time it occurs in the stomach we might as well focus onthat body part. The stomach produces acids to breakdown the food taken in and eventually digest it. Thisparticular acid or also known as gastric acid is very

strong but the stomach and duodenum is able to livewith it since it is protected by a lining of mucus. But ifthat particular lining on the stomach is broken downor eroded thus, the sensitive tissue is below is exposed tothe acid. The acid comes in contact into the wall ofyour stomach or duodenum that damages the partthus, causing ulcer to arise. Many symptoms arise oncea person has peptic ulcer. One is abdominal pains,

bloating and abdominal fullness, waterbash or therush of saliva after diluting acid down the esophagus,nausea, hematemesis or when a person starts vomitingblood, melena and rarely ulcer may direct to a muchcomplicated disease called gastric or duodenalperforation, which eventually may direct to acuteperitonitis. This time it already very painful and theperson would really need to take surgery. This type ofillness may cause many types of complication such asgastrointestinal bleeding being the most commoncomplication, perforation which is basically a whole onthe wall of the stomach, the ulcer continuing to moveand eventually be adjacent to the pancreas and liverand other adjacent organs, scarring and swelling andcancer being the most feared complication. But thepathophysiology of peptic ulcer may involve a muchbraoder value if take into the next level of necessary

actions.


23/49

23

Complications:

y 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.

yy 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 pancreatitis; pai

in this situation often radiates to the back.

y Penetration is when the ulcer continues intoadjacent organs such as the liver and pancreas.[6]

y Scarring and swelling due to ulcers causes


24/49

24

narrowing in the duodenum and gastric outlet

obstruction. Patient often presents with severe

vomiting.

yCancer 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]

y Internal bleeding. Bleeding can occur as slow bloodloss that leads to anemia or as severe blood loss that

may require hospitalization or a blood transfusion.

yy Infection. Peptic ulcers can eat a hole through the

wall of your stomach or small intestine, putting you

at risk of serious infection of your abdominal cavity

(peritonitis).

y Scar tissue. Peptic ulcers can also produce scar tissuethat can block passage of food through the digestive

tract, causing you to become full easily, to vomitand to lose weight.

y Anaemia If the bleeding from the ulcer is slow, youmight not see blood in your vomit or faeces.

However, you may develop anaemia. Anaemia is

when there are too few red blood cells or not enough

haemoglobin in the blood.

y Bleeding Occasionally ulcers can cause the lining oyour stomach or small bowel to bleed. If this happen

suddenly, symptoms may include:

vomiting blood- it may be bright red or like coffee


25/49

25

grains (dark brown bits of clotted blood)

dark faeces that look black or like tar- this is

because the blood from the bleeding ulcer will have

been partially broken down as it makes its waythrough the bowel

If you have any of these symptoms, see your GP

immediately.

&Pyloric stenosis Pyloric stenosis can result if you havea peptic ulcer that causes long-term inflammation inthe lining of your stomach or small bowel. This is anarrowing of the small passage called the pylorus thatlinks your stomach and the first part of your smallbowel. The main symptom of pyloric stenosis is vomiting.

Management :Treatments and drugs

Treatment for peptic ulcers typically involves antibioticsto kill the H. pylori bacterium and other medications treduce the level of acid in your digestive system torelieve pain and encourage healing. You may takeantibiotics for two weeks and acid-reducingmedications for about two months.

If your peptic ulcer isn't caused by H. pylori, you won'tneed antibiotics. Instead, your doctor may recommendtreatments for your specific situation. For instance, ifpain relievers caused your ulcer, your doctor may

recommend a different pain reliever or a different dose.Your doctor may also recommend acid-reducingmedications to allow your ulcer to heal. You may takethese medications for two months or more.


26/49

26

Treatments for peptic ulcer can include:

Antibiotic medications to kill H. pylori. If H. pylori ifound in your digestive tract, your doctor may

recommend a combination of antibiotics to kill thbacterium. Antibiotic regimens are differenthroughout the world. In the United States, antibioticprescribed for treatment of H. pylori includamoxicillin, clarithromycin (Biaxin), metronidazol(Flagyl) and tetracycline. You'll likely need to takantibiotics for two weeks.

Medications that block acid production and promote

healing. Proton pump inhibitors reduce acid byblocking the action of the parts of cells that produceacid. These drugs include the prescription and over-the-counter medications omeprazole (Prilosec),lansoprazole (Prevacid), rabeprazole (Aciphex),esomeprazole (Nexium) and pantoprazole (Protonix).Long-term use of proton pump inhibitors, particularlyat high doses, may increase your risk of hip, wrist and

spine fracture. Ask your doctor whether a calciumsupplement may reduce this risk.

Medications to reduce acid production. Acid blockers also called histamine (H-2) blockers reduce theamount of acid released into your digestive tract,which relieves ulcer pain and encourages healing.Available by prescription or over-the-counter (OTC),acid blockers include the medications ranitidine

(Zantac), famotidine (Pepcid), cimetidine (Tagamet)and nizatidine (Axid).

Antacids that neutralize stomach acid. Your doctormay include an antacid in your drug regimen.Antacids neutralize existing stomach acid and canprovide rapid pain relief. Side effects can include


27/49

27

constipation or diarrhea, depending on the mainingredients.

Medications that protect the lining of your stomachand small intestine. In some cases, your doctor mayprescribe medications called cytoprotective agents thathelp protect the tissues that line your stomach andsmall intestine. They include the prescriptionmedications sucralfate (Carafate) and misoprostol(Cytotec). Another nonprescription cytoprotective agentis bismuth subsalicylate (Pepto-Bismol).

Goal: HP eradication, healing of ulcers, preventionof recurrences and complications of ulcer.

DRUG TREATMENT OF GASTRODUODENALULCERS ASSOCIATED WITH HP.

HP eradication regimen includes use of antibioticsand antacids (level A recommendations). Prolongeantacid use for treatment of ulcers caused by HP is no

recommended (level B recommendations). SuccessfuHP eradication decreases the recurrence rate from 90%to less than 5% a year.1. Seven day regimen:May be taken10-14days,however, there is no data available to show thebenefits of a10- to14-day regimen as compared to a


28/49

28

y seven-day regimenA

Omeprasol (Losek, Omez) from other analoguescurrently recommended is Lansoprasol (Zoton) 20 mgbid or 30 mg bid (in the morning and in the eveningbefore the meal, no later than 8 P.M. with mandatory12-hour interval); capsule should be swallowed, notchewed Klarythromicin (Klacide) 250 mg bid Metronidazole (Trikhopole and other analogues) 500mg bid at the end of the meal. The

drug should not be taken with alcohol; metallic tasteand/or dark urine are possible.

Eradication rate 87-91%.

B

Omeprasol (Losek, Omez) from other analoguescurrently recommended is Lansoprasol (Zoton) 20 mg

bid or 30 mg bid (in the morning and in the eveningbefore the meal, no later than 8 P.M. with mandatory12-hour interval); capsule should be swallowed, notchewed Klarythromicin (Klacide) 250 mg bid Amoxicillin1g bid at the end of the meal.Amoxicillin is recommended in case of priorMetronidazole failure. Metronidazole is recommended

for use in case of hypersensitivity to penicillin.Eradication rate 80-90%.

C

Omeprasol (Losek and analogues) 20 mg bid (in the


29/49

29

morning and in the evening, nolater than 8 P.M. with mandatory12-hour interval)Amoxicillin (Flemoksyn Solutab, Kchikoniil and otheranalogues)1 g/bid at the end of

the mealMetronidazole (Trikhopole and other analogues) 500mg bid at the end of the meal.


D

Pylorid (Ranitidin Bismuth Citrate)400 mg bid atthe end of the meal Klarythromycin (Klacide) 250 mg/bid or tetracycline500 mg four times a day orAmoxicillin1000 mg/bid Metronidazole (Trikhopole and other analogues) 500mg bid during the meal


E

Omeprasol (Losek and analogues 20 mg/bid (in themorning and in the evening, nolater than 8 P.M. with mandatory12-hour interval) Colloid Subcitrate of Bysmuth (Ventrisol, Denol andother analogues) 240 mg/bid 30

minutes before the meal (breakfast or supper) or120mg/q.i.d (first three doses should betaken 30 minutes before breakfast or dinner, or supper.The last two after the meal before going to bed).Withthis medication the tongue and the feces may developdark color; half an hour before and after taking the


30/49

30

medication it is not recommended to drink milk; itshould be used with caution in patients hypersensitiveto aspirin; in case of tinnutis the medication should bediscontinued

Metronidazole 250 mg/qid after the meal orTinidazole 500 mg/bid after the meal Tetracyclin or amoxicillin 500 mg/qid after the meal

Eradication rate in tetracyclin regimen 88-90%, inamoxicillin regimen 80-86%

2. Two-week regimens

A

Ranitidin (Zantak and other analogies)150 mg/bidor Famotidin (Gastrosydyn,Kvamatel, Ulfamyd) 20 mg/bid in the morning and inthe evening (no later than 8 P.M.)

with mandatory1

2-

hour interval; Potassium salt of bismuth citrate gastrostat120mg/qid before the meal Metronidazole 250 mg/qid after meal Tetracyclin hydrochloride 250 mg /qid after meals.Tetracyclin should not be used withdairy products, antacids and medications containingiron; photosensitization in the sunand a rash may develop

Eradication rate 80%

B

Potassium salt of bismuth citrate gastrostat120mg/qid before the meal


31/49

31

Metronidazole 250 mg/qid after meal Tetracyclin hydrochloride 250 mg/qid after meals

Eradication rate 75%

Comments: Resistance may develop in regimens withMetronidazole and Klarythromycin Smoking hinders healing of ulcers and isassociated with increased recurrence rate In absence of symptoms, diagnostic proceduresto confirm successful eradication may be omitted.In case of complicated ulcer, endoscopy is

indicated to confirm the success of the therapy.

Refractory ulcer.The most common causes of refractory and recurrentulcer include1) ineffective eradication therapy;2) unidentified use of NSAID and poor compliancewith medications regimens, incomplete

healing of large ulcers, Zollinger-Ellison syndromeand malignant neoplasms. Should the first stageoftherapy fail, a second stage of eradication therapywith other antibiotics is recommended; term ofthe therapy:14days. Treatment success in the caseof gastric and gastrojejunal ulcers is monitoredendoscopically in eight weeks; in the case ofcomplicated

duodenal ulcer; in4weeks. Use of serologytesting to confirm eradication of HP is not justified,since antibody titer remains elevated even inthe absence of HP.

TREATMENT OF ULCERS CAUSED BYNSAID


32/49

32

NSAID use should be discontinued.Acetaminophen is as effective as NSAID in treatmentof mild/severe arthritis. Routine HP evaluation ofpatients complaining of dyspepsia for NSAID is

currently not recommended. In those cases when NSAIDcannot be discontinued a 20 mg, single dose for fourweeks of Omeprasol (or its analogues) is recommended.Clinical trials have shown that percentage of healingreaches 75-80% for an eight-week treatment.If NSAID can be discontinued, ranitidin (or itsanalogues) is recommended:150 mg/bid for 8 weeks.To prevent peptic ulcer development in patients

taking NSAID with associated risk factors (historyof peptic ulcer or gastric bleeding, older than 75,history of cardiovascular problems), a simultaneousprescription of Misoprostole 200 mg/three

times a day is recommended.

To prevent gastric and duodenal ulcer recurrenceand their complications:

1. Prophylactic therapy on demandstipulatingadministration of one of antacids (Ranitidin,Famotidin, Omeprasol) in a daily dose for 2-3days, and then one half of the dose for twoweeks in case of onset of symptoms characteristicfor the exacerbation of ulceris recommended.If the symptoms of the exacerbationdisappear, the therapy is discontinued. If theypersist, EFGDS and other evaluation proceduresenvisaged by this protocol are indicated.2. Continuous supportive therapy (for a monthor even years) with half the dose of antacid. Forexample, one should take every evening:150mg ofRanitidin or 20 mg Famotidine (gastrosidin,kvamatel, ulfamide). Indications for this


33/49

33

type of therapy include: complications of ulcer (ulcer-related bleedingor perforated ulcer) concurrent ulcerative-erosive esophageal reflux

patients 60+ with annual recurrences of ulcer, despiteadequate therapy

Treatment of GastroduodenalULCERS NOT

ASSOCIATED WITH HP.To exclude or reduce smoking and alcohol use aswell as NSAID use, one of the following drug

combinations and regimens is used:1. Ranitidin (Zantak and other analogues) 300mg a day, single dose at 78 P.M. and antacid(Maaloks, Remagel, Gastrin gel, etc.) as symptomaticmedication2. Famotidin (Gastrosidin, Kvamatel, Ulfamid)40 mg a day at 78 P.M. and antacid (Maaloks,Remagel, Gastrin gel, etc.) as symptomaticmedication

3. Sukralfat (Venter, Sukrat gel)4g a day; moreoften1 g 30 min. before the meal and in theevening two hours after the meal for fourweeks, then 2 g a day for eight weeks.For the treatment of refractory duodenal ulcersnot associated with HP, maximal dose of protonpump inhibitors is recommended (Omeprasol,etc.). Concurrent use of proton pump inhibitors

(PPI) and 2nd type histamine receptors blockers(HRB) is not recommended due to the potentialdecrease in the PPI effectiveness of. In cases ofulcers refractory to HRB-2, PPI is recommended(level A).

Recommendation levels:


34/49

34

A Randomized clinical trials or meta-analysiswith statistically valid resultsB Randomized clinical trials or meta-analysis inwhich clinical outcome is possible but not valid

C Non-randomized clinical trials, the physicianmakes his own decisionDRecommendations of panel, results of separate

clinical observations

The best way to stop any further growth of your stomachulcer is to follow a healthy diet. It must contain non-acidic meals along with liquid meals. Sour agents like

lemon should be strictly avoided in the diet.[20]Younger patients with ulcer-like symptoms are oftentreated with antacids or H2 antagonists before EGD isundertaken. Bismuth compounds may actually reduceor even clear organisms, though the warning labels ofsome bismuth subsalicylate products indicate that theproduct should not be used by someone with anulcer.[clarification needed]

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed aprostaglandinanalogue (Misoprostol) in order to helpprevent peptic ulcers, which may be a side-effect of theNSAIDs.

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

Clarithromycin, Amoxicillin, Tetracycline,Metronidazole) and1 proton pump inhibitor (PPI),sometimes together with a bismuth compound. Incomplicated, treatment-resistant cases, 3 antibiotics(e.g. amoxicillin + clarithromycin + metronidazole)may be used together with a PPI and sometimes with


35/49

35

bismuth compound. An effective first-line therapy foruncomplicated cases would be Amoxicillin +Metronidazole + Pantoprazole (a PPI). In the absenceof H. pylori, long-term higher doses PPIs are often used.

Treatment of H. pylori usually leads to clearing ofinfection, relief of symptoms and eventual healing ofulcers. Recurrence of infection can occur andretreatment may be required, if necessary with otherantibiotics. Since the widespread use of PPI's in the1990s, surgical procedures (like "highly selectivevagotomy") for uncomplicated peptic ulcers became

obsolete.Perforated peptic ulcer is a surgical emergency andrequires surgical repair of the perforation. Mostbleeding ulcers require endoscopy urgently to stopbleeding with cautery, injection, or clipping.

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

these symptoms associated with excessive consumption ofood and drink. Ranitidine is available over thecounter from a pharmacy and works by decreasing theamount of acid the stomach produces allowing healingof ulcers. Zantac tablets containRanitidine150 mg asthe active ingredient which can also be boughtgenerically.

Follow-up after initial treatment

Treatment for peptic ulcers is often successful, leadingto ulcer healing. But if your symptoms are severe or ifthey continue despite treatment, your doctor mayrecommend endoscopy to rule out other possible causesfor your symptoms. If an ulcer is detected duringendoscopy, your doctor may recommend another


36/49

36

endoscopy after your treatment to make sure your ulcerhas healed. Ask your doctor whether you shouldundergo follow-up tests after your treatment.

Ulcers that fail to healPeptic ulcers that don't heal with treatment are calledrefractory ulcers. There are many reasons why an ulcermay fail to heal. These reasons may include:

Not taking medications according to directions.

The fact that some types of H. pylori are resistant toantibiotics.

Regular use of tobacco.

Regular use of pain relievers that increase the risk ofulcers.

Less often, refractory ulcers may be a result of:

Extreme overproduction of stomach acid, such as occursin Zollinger-Ellison syndrome

An infection other than H. pyloriStomach cancer

Other diseases that may cause ulcer-like sores in thestomach and small intestine, such as Crohn's disease

Treatment for refractory ulcers generally involveeliminating factors that may interfere with

healing, along with using different antibiotics.

Surgery and Other Procedures

If bleeding from an ulcer does not stop by usingmedications and supportive care (like fluids and bloodtransfusion), a physician called a gastroenterologistwill perform an endoscopy. He first identifies the ulcer


37/49

37

and the area that is bleeding, then injects medicationsto stop the bleeding and stimulate the formation of ablood clot. If the bleeding recurs or you have aperforated ulcer or an obstruction, surgery may be

required. About 30% of people who come to the hospitalwith a bleeding ulcer need endoscopy or surgery.

Nutrition and Dietary Supplements

Following these nutritional tips may help reducesymptoms:

y Foods containing flavonoids, like apples, celery,cranberries (including cranberry juice), onions,garlic, and tea may inhibit the growth of H. pylori.

y Eat antioxidant foods, including fruits (such asblueberries, cherries, and tomatoes), andvegetables (such as squash and bell peppers).

y Eat foods high in B-vitamins and calcium, such asalmonds, beans, whole grains (if no allergy), darkleafy greens (such as spinach and kale), and seavegetables.

y Avoid refined foods, such as white breads, pastas,and sugar.

y Eat fewer red meats and more lean meats, cold-water fish, tofu (soy, if no allergy) or beans forprotein.

y Use healthy oils, such as olive oil or vegetable oil.y Reduce or eliminate trans-fatty acids, found in

commercially baked goods such as cookies,

crackers, cakes, French fries, onion rings, donuts,processed foods, and margarine.

y Avoid beverages that may irritate the stomachlining or increase acid production includingcoffee (with or without caffeine), alcohol, andcarbonated beverages.


38/49

38

y Drink 6 -8 glasses of filtered water daily.y Exercise at least 30 minutes daily, 5 days a week.

These supplements may also help:

y Probiotic supplement (containing Lactobacillusacidophilus), 5 -10 billion CFUs (colony formingunits) a day--Probiotics or friendly bacteriamay help maintain a balance in the digestivesystem between good and harmful bacteria such asH. pylori. Probiotics may help suppress H. pyloriinfection and may also help reduce side effectsfrom taking antibiotics, the treatment for an H.

pylori infection. Some probiotic supplements mayneed to be refrigerated for best results.

y Vitamin C, 500-1,000 mg1-3 times daily--Onestudy found that taking vitamin C along withtriple therapy allowed the dose of one antibiotic tobe lower. Vitamin C may also be helpful in treatingbleeding stomach ulcers caused by aspirin use.

Choose a healthy diet. Choose a healthy diet full offruits, vegetables and whole grains. Not eatingvitamin-rich foods may make it difficult for your bodyto heal your ulcer.

Consider switching pain relievers. If you use painrelievers regularly, ask your doctor whetheracetaminophen (Tylenol, others) may be an option foryou.

Control stress. Stress may worsen the signs and symptomof a peptic ulcer. Examine your life to determine thesources of your stress and do what you can to addressthose causes. Some stress is unavoidable, but you canlearn to cope with stress with exercise, spending timewith friends or writing in a journal.


39/49

39

Don't smoke. Smoking may interfere with the protectivelining of the stomach, making your stomach moresusceptible to the development of an ulcer. Smoking alsincreases stomach acid.

Limit or avoid alcohol. Excessive use of alcohol canirritate and erode the mucous lining in your stomachand intestines, causing inflammation and bleeding.

Prevention :

You may reduce your risk of peptic ulcer if you:

Protect yourself from infections. It's not clear just how H.pylori spreads, but there's some evidence that it could btransmitted from person to person or through food andwater. You can take steps to protect yourself frominfections, such as H. pylori, by frequently washing yourhands with soap and water and by eating foods thathave been cooked completely.

Use caution with pain relievers. If you regularly usepain relievers that increase your risk of peptic ulcer,take steps to reduce your risk of stomach problems. Forinstance, take your medication with meals. Work withyour doctor to find the lowest dose possible that stillgives you pain relief. Avoid drinking alcohol whentaking your medication, since the two can combine toincrease your risk of stomach upset

Preventing NSAID-related ulcers means findingdifferent medications or alternative approaches to

relieve your pain. Talk to your doctor about youroptions. If you have to take NSAIDs for a long time, yourdoctor may consider prescribing another medication tprevent the development of ulcers. This medicine may


40/49

40

include an H2 blocker or a proton pump inhibitor,which reduce stomach acid.

You can also make lifestyle changes that make you less

prone to get an ulcer from either NSAIDs or H. pylori.

Interventions

1. Assess, report , and record signs and symptoms andreactions to treatment.2. Monitor fluids input and output closely.

3. Administer antacid agents, analgesics, H2-

receptorsantagonists, anticholinergics, sedatives as prescribed,monitor for side effects.4. Monitor clients vital signs and signs of possible GIbleeding or perforation closely.5. Monitor laboratory tests results (CBC, electrolytes, Hblevels) for abnormal values.6. Undertake appropriate intervention in case of GIbleeding, vomiting, or perforation.

7. Provide prescribed diet avoid irritating foods,coffee, etc.8. Prepare client and his family for surgicalintervention if required for recurrent ulcer,hemorrhage, or perforation.9. For client after surgical intervention providepostoperative care and inform about possiblepostoperative complications, such as dumping

syndrome.10. Provide emotional support to client, explain allprocedures to decrease anxiety and to obtaincooperation.11. Instruct client regarding disease progress,diagnostic procedures, treatment and its


41/49

41

complications, home care, daily activities, diet,restrictions and follow-up.

Evaluation

1. Reports increased comfort, decreased anxiety.2. Verbalizes absence of heartburn and pain.3. No evidence of nausea, vomiting, GI bleeding, oracute abdomen.4. Maintains stable vital signs, fluid balance, and bodyweight.5. Laboratory tests results shows no abnormalities.6. No postoperative complications.7. Demonstration of understanding of disease progress,diagnostic and treatment procedures, prevention, andneed for follow-up.

Duodenal Ulcer


42/49

42

A duodenal ulcer is usually caused by an infection witha bacterium (germ) called H. pylori. A 4-8 week courseof acid-suppressing medication will allow the ulcer to

heal. In addition, a one week course of two antibioticsplus an acid-suppressing drug will usually clear the H.pylori infection. This usually prevents the ulcerrecurring again. Anti-inflammatory drugs used to treatconditions such as arthritis sometimes cause duodenalulcers. If you need to continue with the anti-inflammatory drug, then you may need to take longterm acid-suppressing medication.What causes duodenal ulcers?Your stomach normally produces acid to help with thedigestion of food and to kill bacteria. This acid iscorrosive so some cells on the inside lining of thestomach and duodenum produce a natural mucusbarrier which protects the lining of the stomach andduodenum. There is normally a balance between theamount of acid that you make and the mucus defense

barrier. An ulcer may develop if there is an alterationin this balance allowing the acid to damage the liningof the stomach or duodenum. Causes of this include thefollowing:

Infection with Helicobacter pylori


43/49

43

Infection by Helicobacter pylori (commonly just calledH. pylori) is the cause in about19 in 20 cases ofduodenal ulcer. More than a quarter of people in the UKbecome infected with H. pylori at some stage in their life.

Once you are infected, unless treated, the infectionusually stays for the rest of your life. In many people itcauses no problems and a number of these bacteria justlive harmlessly in the lining of the stomach andduodenum. However, in some people this bacteriumcauses an inflammation in the lining of the stomach orduodenum. This causes the defence mucus barrier to bedisrupted (and in some cases the amount of acid to be

increased) which allows the acid to cause inflammationand ulcers.

Anti-inflammatory drugs- including aspirinAnti-inflammatory drugs are sometimes called non-steroidal anti inflammatory drugs (NSAIDs). There arevarious types and brands. For example: aspirin,ibuprofen, diclofenac, etc. Many people take an anti-inflammatory drug for arthritis, muscular pains, etc.

Aspirin is also used by many people to protect againstblood clots forming. However, these drugs sometimesaffect the mucus barrier of the duodenum and allowacid to cause an ulcer. About1 in 20 duodenal ulcersare caused by anti-inflammatory drugs.

Other causes and factorsOther causes are rare. For example, the Zollinger-Ellisonsyndrome. In this rare condition, much more acid than

usual is made by the stomach. Other factors such assmoking, stress, and drinking heavily may possiblyincrease the risk of having a duodenal ulcer. However,these are not usually the underlying cause of aduodenal ulcers.

What are the symptoms of a duodenal ulcer?


44/49

44

y Pain in the upper abdomen just below the sternum(breastbone) is the common symptom. It usuallycomes and goes. It may occur most before meals, orwhen you are hungry. It may be eased if you eat

food, or take antacid tablets. The pain may wakeyou from sleep.

y Other symptoms which may occur include: bloating,retching, and feeling sick. You may feel particularly'full' after a meal. Sometimes food makes the painworse.

y Complications occur in some cases, and can beserious. These include:

oBleeding ulcer. This can range from a 'trickle'to a life-threatening bleed.

o Perforation. This is where the ulcer goes rightthrough ('perforates') the wall of theduodenum. Food and acid in the duodenumthen leak into the abdominal cavity. Thisusually causes severe pain and is a medicalemergency.

What tests may be done?y Endoscopy is the test that can confirm a duodenal

ulcer. In this test a doctor or nurse looks inside yourstomach and duodenum by passing a thin, flexibletelescope down your oesophagus. They can see anyinflammation or ulcers.

y A test to detect the H. pylori bacterium is usuallydone if you have a duodenal ulcer. If H. pylori is

found then it is likely to be the cause of the ulcer.See separate leaflet on Helicobacter Pylori Infectionfor more detail and how it can be diagnosed.Briefly, it can be detected in a sample of faeces, orin a 'breath test', or from a blood test, or from abiopsy sample taken during an endoscopy.


45/49

45

What are the treatments for a duodenal ulcer?

Acid suppressing medicationA 4-8 week course of a drug that greatly reduces the

amount of acid that your stomach makes is usuallyadvised. The most commonly used drug is a proton pumpinhibitor (PPI). These are a class (group) of drugs thatwork on the cells that line the stomach, reducing theproduction of acid. They include: esomeprazole,lansoprazole, omeprazole, pantoprazole andrabeprazole, and come in various brand names.Sometimes a drug from another class of drugs called H2blockers is used. H2 blockers work in a different way on

the cells that line the stomach, reducing the productionof acid. They include: cimetidine, famotidine,nizatidine and ranitidine, and come in various brandnames. As the amount of acid is greatly reduced, theulcer usually heals. However, this is not the end of thestory ...

If your ulcer was caused by H. pyloriNearly all duodenal ulcers are caused by infection with

H. pylori. Therefore, a main part of the treatment is toclear this infection. If this infection is not cleared, theulcer is likely to return once you stop taking acid-suppressing medication. Two antibiotics are needed. Inaddition, you need to take an acid-suppressing drug toreduce the acid in the stomach. This is needed to allowthe antibiotics to work well. You need to take this'combination therapy' (sometimes called 'triple therapy')

for a week.

One course of combination therapy clears H. pyloriinfection in up to 9 in10 cases. If H. pylori is cleared,the chance of a recurrence of a duodenal ulcer isgreatly reduced. However, in a small number of people


46/49

46

H. pylori infection returns at some stage in the future.

After treatment, a test to check that H. Pylori has gonemay be advised. If it is done it needs to be done at least

four weeks after the course of combination therapy hasfinished. In most cases, the test is 'negative' meaningthat the infection has gone. If it has not gone, then arepeat course of combination therapy with a different setof antibiotics may be advised. Some doctors say that forpeople with a duodenal ulcer, this 'confirmation' test isnot necessary if symptoms have gone. The fact thatsymptoms have gone usually indicates that the ulcer

and the cause (H. pylori) have gone. But, some doctorssay it is needed to play safe. Your own doctor will adviseif you should have it. (Note: a test to confirm that Hpylori has gone is usually always recommended if youhave a stomach ulcer.)

If your ulcer was caused by an anti-inflammatory drugIf possible, you should stop the anti-inflammatory drug.This allows the ulcer to heal. You will also normally be

prescribed an acid-suppressing drug for several weeks(as mentioned above). This stops the stomach frommaking acid and allows the ulcer to heal.

However, in many cases the anti-inflammatory drug isneeded to ease symptoms of arthritis or other painfulconditions, or aspirin is needed to protect against bloodclots. In these situations, one option is to take an acid-suppressing drug each day indefinitely. This reduces theamount of acid made by the stomach, and greatlyreduces the chance of an ulcer forming again.

SurgeryIn the past, surgery was commonly needed to treat aduodenal ulcer. This was before it was discovered that H.


47/49

47

pylori was the cause of most duodenal ulcers, and beforemodern acid-suppressing drugs became available.Surgery is now usually only needed if a complication ofa duodenal ulcer develops such as severe bleeding or a

perforation.

Zollinger-Ellison Syndrome

What is Zollinger-Ellison Syndrome?

Zollinger-Ellison Syndrome is a rare condition thatcauses severestomach ulcers. It is characterized bytumors (gastrinomas) in the body. The tumors mostcommonly form in thepancreasand duodenum. Thetumors cause ulcers because they secrete a substance

called gastrin, which stimulates excessive acid secretionby thestomach.

Ulcers associated with Zollinger-Ellison Syndrome areoften difficult to control. They are more persistent andless responsive to treatments than usual ulcers are.


48/49

48

Zollinger-Ellison Syndrome may occur at any age, but itis more likely to appear between the ages of 30 and 60years old.

Symptoms of Zollinger-Ellison SyndromeThe most common symptoms of Zollinger-EllisonSyndrome are:

y diarrheay abdominal painy bleedingy fatigue and weaknessy yellow fat in stool

How serious is Zollinger-Ellison Syndrome?

Zollinger-Ellison Syndrome is a serious condition. Thetumors may spread to the lymph nodes and liver. Theearlier it is detected, the better the chances of recovery.

Treatment options for Zollinger-Ellison Syndrome

Zollinger-Ellison Syndrome can be treated. If the tumorsare big enough, the doctor may choose to performsurgery to remove the tumors. If the tumors are small ortoo numerous to be removed, the doctor will probablyprescribe acid-reducing medication. The patient willprobably have to take the medication for a long period

of time.In very severe cases of Zollinger-Ellison Syndrome, theentire stomach may have to be surgically removed.

How is Zollinger-Ellison Syndrome Diagnosed?


49/49

Your doctor will perform blood tests, an upper endoscopeexamination and barium x-ray to determine if hethinks you have Zollinger-Ellison Syndrome.

Documents

Peptic Ulcermazher