Peptic Ulcer Disease (PUD)

IM

DR WAQAR

OBJECTIVES

By the end of this lecture, student should know:

• Difference b/w PUD & dyspepsia
• Etiologies
• Signs and Symptoms
• Investigation for H. Pylori and peptic ulcer
• Treatment of Peptic ulcer
• Know which tests to do after treatment
• What is Zollinger Ellison Syndrome

CASE 1

25 year old male Pain in epigastric area, off and on since 2 months. Relieved with food Smoker, on NSAIDS since long time Very stressful job Physical examination normal Name some differentials

Case 2

50 year old female Epigastric pain since 3 months off and on. More after eating Pale stools which are difficult to flush Weight loss of 10 kg in 3 months Chronic alcoholic. Serum triglycerides very high Jaundice present What is your differential?

Dyspepsia

What is Dyspepsia ?

The term “ dyspepsia” is a broad term and includes any of the following:

• Heart burn
• Food related discomfort in the upper abdomen
• Nausea, gas etc
• Feeling of fullness after eating a little

Every dyspepsia patient does not need urgent & detailed investigations. However, presence of any of the following warrants urgent workup (alarm symptoms)

• Dysphagia
• Weight loss
• Severe Vomiting
• Severe anorexia
• Hematemesis
• Melena

PEPTIC ULCER

Definition:

It is a break in the gastric /duodenal mucosa, extending down to the muscularis layer.

EROSIONS: Superficial breaks in the mucosa alone, not extending deep.

Most common sites of peptic ulcers:

• Duodenal bulb (most common)
• Lesser curvature
• Antrum of the stomach

SOME GENERAL POINTS

Feature	Duodenal Ulcers	Gastric ulcers
Frequency	Much more common than gastric ulcers	Less common
Location	Usually in the duod. bulb(1st part)
Malignancy	Almost never malignant	May be malignant
Pain with eating	Eating relieves pain	Eating worsens the pain
Age	Typically younger	Usually above age 50

ETIOLOGY OF ULCERS

1. Helicobacter Pylori infection -⇒ Most Common
2. NSAID/ Aspirin use ⇒ Most Common
3. Hyperacidity states (eg Zollinger Ellison syndrome)
4. Biphosphonates ( medicines used in osteoporosis)
5. Stress
6. Alcohol, dietary factors & smoking may aggravate the symptoms.

SO: In patients with peptic ulcers, the first 2 things to rule out are:

1. H. Pylori infection (by tests)
2. NSAID use (by history)

Some points about H. Pylori

• It is a bacterium infecting the gastric & duodenal mucosa
• 2/3rd of the world population is infected
• Poor hygienic conditions → more chances of infection
• Can cause “no” symptoms OR erosions, gastritis, ulcers

***Points about ulcer producing drugs ***

1. Long term use of aspirin & ‘traditional’ NSAIDs (diclofenac, ibuprofen etc), increases the risk of peptic ulcers. ( gastric more than duodenal)
2. Use of these meds in ulcer patients → high risk of complications
3. COX 2 inhibitors(which are also NSAIDs) have much less risk of peptic ulcer disease ( eg celecoxib). They may be called “gastro-protective” )
4. Long term steroid use increases ulcer risk

So, ulcer producing drugs are:

• NSAIDs
• Aspirin
• Steroids

SIGNS & SYMPTOMS of ULCERS

1. Asymptomatic: 70% of patients can be totally asymptomatic, specially those on NSAIDs.

2. Epigastric pain:

   • Classic symptom
   • Usually a dull ache
   • Relieved by antacids
   • Food relieves pain in DU

3. Nausea, belching, heartburn, bloating etc. ( dyspeptic symps).

4. Physical exam is usually normal ( may be mild epig. tenderness)

Clinical S/S can not distinguish between DU & gastric ulcer

INVESTIGATIONS

In uncomplicated ulcers, basic investigations like CBC and chemistry are usually normal ( Hb may be low in bleeding ulcers)

The 2 “specific” investigations in peptic ulcer patients are:

1. Endoscopy (confirms ulcer)
2. H. Pylori testing (Barium studies are no longer done)

ENDOSCOPY

• It is the best investigation to diagnose ulcers
• During endoscopy, biopsy of the ulcer is always taken and sent for H. Pylori testing(CLO TEST)
• In case of gastric ulcer, biopsy is also sent to rule out carcinoma(some gastric ulcers can be malignant)
• DU are never malignant.

Endoscopic views

H. Pylori testing

4 commonly used methods of detecting H. Pylori:

• Urea breath test (most frequently used with 95% sensitivity)
• Stool antigen test (most frequently used with 95% sensitivity)
• CLO test (after biopsy)
• Serum antibody titers ⇒ (very frequently used but low specificity. Can be done if 1,2 & 3 are not available)

Before understanding the urea breath test and CLO test , remember the following: H. Pylori produces the enzyme “ urease” which can split urea into NH3( ammonia ) and CO2

              urease 
   UREA        -->         NH3  +  CO2

1. Urea breath test:

• Pt. ingests urea tablets which contain C₁₄
• H. Pylori urease splits urea into NH3 & CO2
• CO2 (which contains C14) is exhaled through the lungs and collected in a bag
• Results are very quick ( 15 min)

Tablets & bag ( full kit)

2) Stool Antigen test: H. Pylori antigens are checked in the stool.

3) CLO test ( rapid urease test):

• Biopsy of the ulcer taken during endoscopy
• Sample is placed in a solution which contains urea
• Urease of H. Pylori splits urea & releases NH3 → color of the solution changes

Before doing 1, 2 and 3, stop PPIs for 14 days

STEPWISE MANAGEMENT

S/S SUGGESTING PEPTIC ULCER DISEASE

Patient less than 60 yrs. & no alarm symptoms( wt loss, dysphagia, hematemesis, melena) → Endosc. not LAAZIM. Check for H. pylori & treat. If neg., give PPIs for 1 month

If age more than 60 OR alarm symps. MOJOOD → endoscopy & H. pylori testing. Then treat accordingly

MANAGEMENT OF PUD

• Avoid smoking
• Avoid aspirin, NSAIDs and steroids
• No specific dietary restrictions but avoid things which cause hyperacidity (spices,caffiene)

MEDICAL TREATMENT

Symptomatic	H. Pylori treatment
1) Antacids (PPIs etc) 2) Mucosal protective agents	treat the pathogen directly

MEDICINES For PUD

Antacids

• PPIs ( eg. omeprazole)
• H2 antagonists ( Zantac)
• Aluminium OH/Mg OH( tabs, liq) ( GAVISCON)

2) Mucosal protective agents ( Bismuth)

3) H. Pylori eradication meds.

1) Antacids

a) PPIs are the most effective & safest

• Omeprazole, es-omeprazole, pantoprazole
• Once daily before breakfast
• Usually given for 1 month to heal the ulcer, then stopped
• Long term use only in some patients

b) H2 receptor antagonists:

• Ranitidine( zantac), Nizatidine, famotidine
• Zantac has been withdrawn in the U.S.

c) Aluminium/Mg hydroxide: provides acute symptomatic relief of ulcer pain. ( Gaviscon tabs / syrup)

2) Mucosal protective agents (Bismuth) :

They “coat” the ulcer

3) Treatment of H. Pylori

Till recently, the following was the most common regimen used but now it is not the first line therapy:

Amoxicillin + Clarithromycin + PPI (all for 10 to 14 days)

FIRST LINE REGIMENS (American coll. of Gastroentero.)

QUADRUPLE THERAPIES 1) 14 Days

• PPI bid
• Bismuth tablets (4 times daily) (14 days)
• Tetracycline tabs( 4 times daily) (14 days)
• Metronidazole (Flagyl) tid (2 antacids + 2 antibiotics)

OR

2) 14 Days

• PPI (bid) (14 days)
• Amoxicillin(bid) (14 days)
• Flagyl
• Clarithromycin (1 antacid + 3 antibiotics)

HOW TO REMEMBER?

Patchi Chocolate For Ahmed

• P: PPI
• C: Clarithromycin
• F: Flagyl
• A: Amoxicillin

These regimens have a high eradication rate and low recurrence of symptoms After this treatment, continuous PPI treatment is not needed in most cases( some may need)

To confirm eradication, do one of these:

• a) Urea breath test after 1 month
• b) H. Pylori stool antigen test after 1 month

Failure to eradicate with these regimens or recurrence of symptoms may need other regimens or surgery Never use the same regimen twice

Ulcer prevention in special situations

Patients on long term NSAIDs, aspirin or corticosteroids → high risk of PUD → so, give prophylactic PPI & use gastroprotective NSAIDs( eg celecoxib)

Hospitalised patients → more chances of stress ulcers → so PPI routinely given

Complications of PUD

• Bleeding (most common complication)
• Perforation (can lead to ? )
• Ulcer in the pylorus can become fibrosed/scarred → gastric outlet obstruction → persistent vomiting

ZOLLINGER ELLISON SYNDROME

It is a syndrome due to a gastrin secreting tumor (usually in the pancreas or duodenum).

Excess gastrin → hyperacidity → duodenal ulcers & diarrhea

When to suspect:

• Ulcers not responding to usual treatment
• ***Large ulcer ***
• Multiple ulcers

DIAGNOSIS:

• Fasting serum gastrin levels : High
• Serum gastrin levels after giving i.v. “secretin” ( secretin stimulation test). In gastrinoma, further rise in serum gastrin levels

Rx: Surgical removal of the tumour

RAPID FIRE QUESTIONS

1. Difference between ulcer & erosion? ulcer is deeper; superficial

2. Name 2 most common causes of peptic ulcer? Nsaids, h pylori

3. Which medicines can cause ulcer? biphosphatase nsaids

4. Name 4 alarm symptoms in dyspepsia patient, where endoscopy is LAAZIM? hematemisis, melena, weightloss, vomitting

5. Name 3 most common areas where ulcers occur? duodenum pul, epigastric, pylorus

6. Food worsens the pain in which ulcer? gastric when you eat food, duodenal better

7. Which ulcers can be malignant, duod or gastric? commonly in gastric

8. Symptoms suggesting ulcer disease. What are the next 2 steps to do? Endoscopy, H. Pyolri testing

9. H. Pylori can cause what? gastritis, Ulcer gastric/duodenal, asymptomatic

10. Which NSAIDs are gastro-protective? ?

11. Can ulcer patients be asymptomatic? yes

12. Name the 4 tests for H. Pylori? Which is NOT the best? Urea breath test, serum anti body titers, …, …

13. Which enzyme is produced by H. Pylori? urease

14. Patient is taking PPI form before. You want to do H.Pylori test. Whats the first step to do? 2 weeks stoppage before testing

15. What are the “symptomatic” treatments for peptic ulcer disease? antiacids, PPI, Bismo

16. Which drug was withdrawn in the U.S? tidine..

17. Treatment of H. Pylori is “3 drugs for 10 days”, right or wrong? wrong - 4 drugs for 2 weeks

18. Treatment of H. Pylori? Name any 1 regimen? choclate…

19. After treatment, which test to do to confirm eradication? When to do? Urea breath test - after month

20. When to give prophylactic PPIs? Name any 2 situations? Nsaids

21. 3 complications of ulcer disease? Perforation, malabsorption

22. What is high in Zollinger Ellison syndrome? gastrin secretin

23. When to suspect this syndrome? large ulcer, multiple

24. Rx of Zollinger? Surgery

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SURGE

• Peptic ulcers are found approximately four times as often in the duodenum than in the stomach
• Duodenal ulcers are more common in men
• Gastric ulcers equally affect men and women
• Ulcers are found at all ages
• More common with increasing age
• Whilst acid attack is a marked feature of duodenal ulcer (DU),
• impaired mucosal resistance appears to be more important for gastric ulcer.

DUODENAL ULCER: Risk Factors:

• Cigarette smoking, stress, NSAIDs, corticosteroids and infection with H. Pylori

• NSAIDs—Deplete endogenous mucosal prostaglandins making the mucosa more susceptible to ulceration.

• Smoking—Increases acid secretion, impairs ulcer healing, accelerates gastric emptying and decreases pancreatic bicarbonate secretion.

• H. pylori—Over 90 percent patients with a duodenal ulcer have this organism

Clinical Features: DU

1. Epigastric pain—Most frequent symptom, appears in empty stomach and relieved by taking food.

2. Appetite is good.

3. Malignancy almost never occurs.

4. Vomiting not so common.

5. Periodicity comes and goes in a 4 to 6 months cycle.

6. Duration of attack—A month or two.

Diagnosis :

• Endoscopy—This has replaced Ba–meal examination as the mainstay of diagnosis. In addition to confirming the presence of peptic ulceration, endoscopy allows esophageal disease to be excluded, may reveal unsuspected pathology and allows gastric ulcers to be biopsied to exclude malignancy.

• USG—This is advisable to exclude gallstones as cholelithiasis and peptic ulceration often coexist and share common symptoms.

Differential Diagnosis

1. Chronic gastric ulcer.
2. Chronic cholecystitis.
3. Chronic amebiasis and worm infestation.
4. Chronic pancreatitis.
5. Chronic appendicitis.
6. Intestinal tuberculosis.

Treatment:

Medical Measures

1. Cessation of smoking and intake of NSAIDs, steroids, etc.

2. A period of bed rest and a change to less stressful life style and small frequent meals without spices (i.e. No hurry, curry and warry).

3. Drug therapy: a. Antacid (liquid)—1, 2 and 3 hours after meal. b. H2 Blocker—Famotidine 40mg/day. c. Proton pump inhibitor—e.g. omeprazale 20mg/day. d. Cytoprotective agent, e.g. sucralfate, colloidal bismuth, etc.

Peptic ulcer perforation

‘Boardlike rigidity’ of diffuse peritonitis However, in the elderly and the critically ill presentation can be atypical. Subdiaphragmatic free gas on a plain erect chest X-ray is diagnostic. The availability of Helicobacter pylori eradication regimens and potent proton-pump inhibitors alleviate patients’ ulcer diathesis without the need for a definitive acid-reducing procedure. A simple omental patch repair and thorough peritoneal toileting to be done during the emergency operation. The only exception is giant duodenal perforations (>2 cm), not be amenable to a simple patch repair

Z OSPE EX Erect chest radiograph showing right subphrenic free gas shadow associated with a perforated peptic ulcer.

A small perforation at the juxtapyloric area

Pedicle omental patch (Graham) repair on the perforation site secured with absorbable sutures

Surgical Treatment:

Indications:Z

1. Failure of medical treatment, i.e. failure of the ulcer to heal or recurrence, after rigid medical treatment (6 months for duodenal ulcer and 3 to 4 weeks for gastric ulcer).
2. Appearance of complications, e.g. pyloric stenosis, repeated hemorrhage.
3. Ulcer of > 5 years standing.
4. Very large ulcers (> 5 cm size).

Type of operation:

1. Truncal vagotomy with a drainage procedure (TV + D) e.g. pyloroplasty or gastrojejunostomy.

2. Truncal vagotomy and antrectomy, bowel continuity is maintained by Billroth I or Billroth II anastomosis. Billroth II gastrectomy has higher mortality and morbidity.

3. Highly selective vagotomy (HSV) without any drainage procedure.

BillrothZ

GASTRIC ULCER

Risk Factors :

• Tobacco, alcohol and H. pylori infection.

• 10 percent of people taking NSAIDs, suffer from acute gastric ulcer.

• Gastric ulcer frequently develops in degenerate and aged gastric mucosa.

Site Gastric ulcer is most frequently seen near the incisura, a constant notch in the lower part of lesser curvature.

Age/Sex Gastric ulcers occur most commonly in elderly women with the highest incidence between 55 and 60 years of age.

Clinical Features:

• Pain occurs soon (15–30 min) after eating, which is the precipitating factor unlike duodenal ulcer.

• Relieving factor—vomiting.

• There may be loss of weight and hematemesis is more common than melena.

• Diagnosis by endoscopy and biopsy.

A good clinical rule is to suspect initially that every gastric ulcer is malignant.

Treatment:

• Medical treatment is effective and is the first line of approach for most patients. Surgery is usually reserved for cases where medical treatment fails or if there are complications such as bleeding, perforation, or obstruction.

• Combined gastric ulcer + Duodenal ulcer, treatment of choice is partial gastrectomy that includes the entire antrum and the ulcer plus truncal vagotomy of both vagus nerves.

• For gastric ulcer–Treatment is only partial gastrectomy (Billroth-1) that includes the entire antrum and the ulcer without vagotomy.

• Billroth-I is preferred to Billroth-II operation if the duodenum is not badly deformed.

Complications of gastric ulcer:

• Complications are same as in case of chronic duodenal ulcer. But bleeding occurs more commonly and perforation less frequently than duodenal ulcers.

• An unusual complication of perforation is a gastrocolic fistula, when ulcers on the greater curvature penetrate the colon. Here surgical intervention is necessary.

• Delayed healing, are more common in smokers than in non-smokers.

• Obstruction

• Weight loss

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Therapeutics

Peptic Ulcer Definition

ulcer which occur in presence of acid and pepsin (penetrate muscularis mucosa). It is defined as a chronic inflammatory condition characterized by ulceration in regions of the upper gastrointestinal tract where parietal cells secrete pepsin and hydrochloric acid. The most common sites are the duodenum and stomach.

An ulcer of the alimentary tract mucosa, usually in the stomach or duodenum, & rarely in the lower esophagus, where the mucosa is exposed to the acid gastric secretion

It has to be deep enough to penetrate the muscularis mucosa

Other types Definitions: Ulcers Erosion

Types:

1-Acute : ( superficial gastric erosions): due to

• ulcerogenic drugs e.g NSAID and aspirin
• Stress ulcer e.g MI, hypotension due to hemorrhage….etc.

2-chronic ulcer

Mode of transmission:

Transmission is from person to person, and an important mode of spread may be gastro-oral (ie, through exposure to vomitus or saliva).

Epidemiology:

H.pylori infection is commoner in developing countries and is associated with low socioeconomic standards worldwide. The majority of infections are probably acquired in childhood.

Etiology:

Major causes of peptic ulcer: The majority of PUD patients are  H. pylori infected

• H. pylori infection (previously discussed) ( 70-80%)
• Aspirin and other Non steroidal anti-inflammatory drugs (NSAIDs). Most of drug induced ulcers are dose related. They decrease mucosal resistance (main factor in GU
• Acid hypersecretory states such as Zollinger-Ellison syndrome. (gastrin hormone production)
• Up to one-fourth of ulcers are idiopathic.
• excess vagal stimulation (stress and anxiety)
• decreased gastrin and histamine  destruction as in liver cell failure and hepatic cirrhosis
• allergic conditions (histamine)

N.B.:Z Cyclooxygenase-2 (COX-2) inhibitors: Celecoxib, rofecoxib, and valdecoxibe are NSAIDs that selectively inhibit cyclooxygenase-2 (COX-2)-the principal enzyme involved in prostaglandin production at sites of inflammation-while sparing cyclooxygenase-1 (COX-1), the principal enzyme involved in the synthesis of prostaglandins important in gastric cytoprotection.

Regulation of HCl secretion

Best general drug is proton pump inhibitor - Omeprazole

Clinical sequelae:

1. Although chronic H pylori infection with gastritis is present in 30-50% of the population, the majority are asymptomatic and suffer no sequel.

2. Peptic ulcer disease (especially duodenal ulcer); however, only J 5% of people with chronic infection develop a peptic ulcer.

3. Chronic H pylori gastritis

4. Increased risk of gastric adenocarcinoma and low-grade B cell gastric lymphoma (mucosa-associated lymphoid tissue lymphoma; MALToma).

Clinical picture of peptic ulcer:

(A) Typical presentations: Symptoms: Patients can be asymptomatic or have anorexia, nausea, vomiting, heartburn or epigastric pain.

Ulcer pain or ulcer dyspepsia:

Feature	DU (Duodenal Ulcer)	GU (Gastric Ulcer)
Etiology	Contact of acid with exposed nerve endings in the base of the ulcer	Contact of acid with exposed nerve endings in the base of the ulcer
Character	Deep seated burning sensation (may be dull, colicky, or stabbing)	Deep seated burning sensation (may be dull, colicky, or stabbing)
Time	pain occur 0 .5- 2 hours after meal (hunger pain) to buffer hyperacidity. Also occur at night (nocturnal pain which awake patient at midnight)	0.5-1 hour after meal
Site	Epigastric pain to the right of middle line	Epigastric pain to the left of middle line
Factors that increase pain	Hunger, irritant foods, smoking, stress, tea, coffee, drugs	Food, … (other factors TBD)
Factors that decrease pain	Alkalies, eating	Alkalies, vomiting
Signs	Localized tenderness at the site of pain (right of middle line)	Localized tenderness at the site of pain (left of middle line)
Appetite	Weight gain	Weight loss

(B) Atypical presentation:

• Painless ulcer: may be (bleeding, perforation, DM….etc
• Complicated ulcer: 1- GIT bleeding: may be —Occult blood in the stool -severe hemorrhage with haematemesis and melena 2- Perforation 3- Malignancy

The differences between DU and GU can be slight, making differentiation difficult based on symptoms alone so, the accurate diagnosis depends on radiological (barium meal) or endoscopic visualization of the ulcer.

Physical examination

It is often normal in uncomplicated peptic ulcer disease. Localized epigastric tenderness to deep palpation may be present. Pointing tenderness in the epigastrium in D.U.

Signs of complication:

• Pallor due to anemia due to chronic blood loss.
• Haematemsis and melena.
• Gastric carcinoma in gastric ulcer.

Pathophysiology of peptic ulcer :

Normally there is balance between : 1) Defensive mechanism in the stomach due to

• mucosa secrete mucous and bicarbonate
• mucosa rapidly replaces damaged epithelial cells
• mucosa synthesizes PGE1 and PGE2 which (stimulate synthesis and secretion of mucous and bicarbonate and increases gastric blood flow)

So, mucous and bicarbonate form protective gel like over the mucosa which with the epithelial cells tight junction form mucosal barrier which prevent (back diffusion of acid (H) , also Na and K diffusion to gastric mucosa)

2)Aggressive factors in the stomach:

• secretion of HCL and pepsin(proteolytic enzyme)

• infection of the stomach specially in the duodenum with helicopacter pylori (G-ve bacilli)

• Ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter. Ulcers

• occur five times more common in the duodenum than the stomach. Over 95% of the duodenal

• ulcers are in the bulb or pyloric channel.

Incidence: Peptic ulcer disease (PUD) is a common disorder that affects millions of individuals worldwide

Although ulcers can occur in any age group, duodenal ulcers most commonly occur between the ages of 30 and 55, whereas gastric ulcers are more common between the ages of 55 and 70.

Investigations:

1- Laboratory findings:

• Microcytic hypochromic anemia may occur with blood loss from a bleeding ulcer.
• Leukocytosis suggests ulcer penetration or perforation.
• An elevated serum amylase in a patient with severe epigastric pain suggests ulcer penetration into the pancreas.
• A fasting serum gastrin level to screen for Zollinger-Ellison syndrome is needed in some patients with recurrent intractable ulcers .

2-Endoscopy:

• Upper endoscopy is the procedure of choice for the diagnosis.

• Duodenal ulcers are virtually never malignant and do not require biopsy. However, biopsies of gastric ulcers are performed to rule out malignancy.

•Imaging: Barium upper gastrointestinal series has limited accuracy .

•Testing for H pylori: (Discussed previously)

Diagnosis:

A. Noninvasive testing for H. pylori:

1. Serologic ELISA tests have sensitivity and specificity of over 90%. Positive serologic tests do not necessarily imply ongoing active infection. After H. pylori eradication with antibiotics, antibody levels decline to undetectable levels in 50% of patients by 12-18 months.

2. A fecal antigen immunoassay has excellent sensitivity and specificity (90%). A positive test is indicative of active infectionZ

3. The 13C-urea and 14C-urea breath tests also have excellent sensitivity and specificity (90%), and a positive test is indicative of active infection. However, their greater cost makes them less attractive than other noninvasive tests in most clinical settings.

B. Endoscopic testing for H. pylori: Endoscopically obtained gastric biopsy specimens can be obtained for detection of H pylori by testing for urease production.

Histologic assessment of biopsies from the gastric antrum and body is more definitive.

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Complications of peptic ulcer:

1. Hemorrhage: Is the most common complication, it is an emergency situation and is lethal in I 0% of patients, the mortality increases with age. It presents with anemia with occult blood in stools, hematemesis, vomiting of coffee ground material, melena or with shock.

Treatment: The patient needs to be admitted to the ICU, resuscitated by fluids and blood. Endoscopy upper GI to know the cause of the bleeding, should b e done Intravenous proton pump inhibitors.

2. Perforation:

• It usually presents with sudden onset of severe abdominal pain; ileus and board like rigidity of the abdominal wall.

• The first presentation may be shock and septicemia. Polymorph nuclear leukocytosis and raised serum amylase may be found.

• Plain X-ray abdomen in the erect position may show air under the diaphragm.

Management: Nasogastric tube to empty the stomach and prevent further peritoneal soiling. IV fluids and broad spectrum antibiotic, followed by surgical closure and omental patch.

3. Penetration: Into the pancreas or the biliary system presents with increasing severity of the pain with radiation to the back and symptoms and signs of pancreatitis and cholangitis.

4. Gastric outlet obstruction:

• It presents with epigastric fullness, vomiting of foul odor of previously ingested food with alkalosis , loss of weight is seen in longstanding cases.
• The obstruction may be due to edema and inflammatory reaction around the ulcer.
• Barium meal and endoscopy are diagnostic.

Management: Naso-gastric suction for one week combined with IV fluid replacement and proton pump inhibitors. The most common cause is fibrosis and scarring and this needs endoscopic balloon dilatation or surgery.

5. Malignant change in gastric ulcer

Eradication therapy:

All patients with duodenal and gastric ulcers should have H. pylori eradication therapy. - There are several protocols for eradication but the most widely accepted is done by one week triple therapy including:

• Omeprazole (20 mg bid)+ Clarithromycin (500 mg bid) + Metronidazole (500 mg bid or amoxicillin (1 gm bid)
• NB: However recurrence is common.