A 36-year-old man presented with a 2-month history of epigastric pain mainly after meals and sometimes awakening at night due to burning pain, which was relieved by drinking milk. The summary examines peptic ulcer disease, including that it is caused by H. pylori infection or NSAID use. Diagnosis involves testing for H. pylori via a urease test or other methods. Treatment involves acid suppression with PPIs combined with clarithromycin and amoxicillin antibiotics for 2 weeks to eradicate H. pylori infection.

1. PEPTIC ULCER
DISEASE
Dr. HUSSEIN SAAD
Assistant Professor and Consultant, MRCP(UK)
FAMILY and COMMUNITY MEDICINE
College of Medicine
King Saud University
26/09/2016

2. • Aetiology
• Presentation
• Approash:
 Diagnosis
 H pylori
 Management

3. Case
• A 36-year-old man, smoker, presents with 2
months H/O epigastric pain mainly post meals.
He sometimes awake by night because of
burning pain to which he used to drink milk to
relieve the pain.
• No vomiting
• He has no H/o any chronic illnesses
• No H/o of drugs

4. Peptic ulcer
 Refers to erosion of the mucosa lining any portion of the G.I. tract.
 It is defined as: A circumscribed ulceration of the gastrointestinal
mucosa occurring in areas exposed to acid and pepsin and most often
caused by Helicobacter pylori infection. (Uphold & Graham, 2003)
 Gastric ulcer : the ulcer that occurs in the stomach lining ,some of them
may be malignant
 Duodenal ulcer : most often seen in first portion of duodenum (>95%)
Peptic Ulcer Disease (PUD)
Definition

5. Peptic ulcer disease

6. Peptic Ulcer Disease
Pathogenesis :

7. Aetiology
•H pylori infection
•Drugs like NSAIDs, Aspirin or
Corticosteroids
•Smoking
•Stress like trauma, surgery
•Excess gastrin secretion

8. ETIOLOGIC FACTORS OF PUD

9. Presentation
• Gastric and duodenal ulcers usually cannot be
differentiated based on history alone.
• Epigastric pain is the most common symptom.
• It is characterized by a burning sensation and occurs
after meals—classically, shortly after meals with
gastric ulcer and 2-3 hours afterward with duodenal
ulcer.

10. Presentation
• Food or antacids relieve the pain of duodenal ulcers
but provide minimal relief of gastric ulcer pain.
• Duodenal ulcer pain often awakens the patient at
night.
• About 50-80% of patients with duodenal ulcers
experience nightly pain, as opposed to only 30-40% of
patients with gastric ulcers and 20-40% of patients
with nonulcer dyspepsia (NUD).

11. Case
• A 36-year-old man, smoker, presents with 2
months H/O epigastric pain mainly post meals.
He sometimes awake by night because of
burning pain to which he used to drink milk to
relieve the pain.
• No vomiting
• He has no H/o any chronic illnesses
• No H/o of drugs

12. Presentation
• Pain with radiation to the back is suggestive of a
posterior penetrating gastric ulcer complicated by
pancreatitis.
• Patients who develop gastric outlet obstruction as a
result of a chronic, untreated duodenal ulcer usually
report a history of fullness and bloating associated
with nausea and emesis that occurs several hours
after food intake.

13. Presentation
Other possible manifestations include the following:
Dyspepsia, including belching, bloating, distention, and
fatty food intolerance
Heartburn
Chest discomfort
Hematemesis or melena resulting from gastrointestinal
bleeding. Melena may be intermittent over several days or
multiple episodes in a single day.
Symptoms consistent with IDA (eg, fatigue, dyspnea).
NSAID-induced gastritis or ulcers may be silent,
especially in elderly patients.

14. Alarm Features
Warrant prompt gastroenterology referral:
• Bleeding or anemia
• Early satiety
• Unexplained weight loss
• Progressive dysphagia or odynophagia
• Recurrent vomiting
• Family history of GI cancer

15. Serum Gastrin Level
• A fasting serum gastrin level should be obtained in certain
cases to screen for Zollinger-Ellison syndrome.
• Patients with multiple ulcers
• Strong family history of PUD
• Peptic ulcer associated with diarrhea, steatorrhea, or
weight loss
• Peptic ulcer not associated with H pylori infection or
NSAID use
• Peptic ulcer associated with hypercalcemia or renal stones
• Ulcer refractory to medical therapy
• Ulcer recurring after surgery
•

16. Differential Diagnoses
• Acute Cholangitis
• Acute Coronary Syndrome
• Acute Gastritis
• Cholecystitis and Biliary Colic
• Chronic Gastritis
• Diverticulitis
• Esophagitis
• Gallstones (Cholelithiasis)
• Gastroesophageal Reflux Disease
• Inflammatory Bowel Disease
• Viral Hepatitis

17. Types of Ulcer
• Benign ulcers tend to have a smooth, regular, rounded
edge with a flat smooth base and surrounding mucosa
that shows radiating folds.
• Malignant ulcers usually have irregular heaped-up or
overhanging margins. The ulcerated mass often protrudes
into the lumen, and the folds surrounding the ulcer crater
are often nodular and irregular.

18. Benign Ulcers

19. Malignant Ulcer

20. Helicobacter pylori
 Gram negative, Spiral bacilli
 Spirochetes
 Do not invade cells – only mucous
 Breakdown urea - ammonia
 Break down mucosal defense
 Chronic Superficial inflammation

21. H pylori Testing
• Testing for H pylori infection is essential in all
patients with peptic ulcers.
No acid
No ulcer
OLD TESTAMENT
No HP No ulcer
NEW TESTAMENT

22. Rapid Urease Tests
Are considered the endoscopic diagnostic test of choice.
The presence of H pylori in gastric mucosal biopsy
specimens is detected by testing for the bacterial product
urease.
The kit contains a combination of a urea substrate and a pH
sensitive indicator. One or more gastric biopsy specimens
are placed in the rapid urease test kit. If H pylori is present,
bacterial urease converts urea to ammonia, which changes
the pH, resulting in a color change.

23. Urease Test

24. Histopathology
• Often considered the criterion standard to establish a
diagnosis of H pylori infection , if the rapid urease test
result is negative and a high suspicion for H pylori persists
(presence of a duodenal ulcer).

25. Urea Breath Tests (13C and14C)
• Detect active H pylori infection by testing for the
enzymatic activity of bacterial urease.
• In the presence of urease produced by H pylori, labeled
carbon dioxide (heavy isotope, carbon-13, or radioactive
isotope, carbon-14) is produced in the stomach, absorbed
into the bloodstream, diffused into the lungs, and exhaled.

26. Fecal Antigen Testing
• Identifies active H pylori infection by detecting the
presence of H pylori antigens in stools.
• This test is more accurate than antibody testing and is
less expensive than urea breath tests.

27. Antibodies
• (Immunoglobulin G [IgG]) to H pylori can be measured in
serum, plasma, or whole blood.
• Not effective in follow up after eradication.

28. Approach Considerations
Treatment of peptic ulcers varies depending on:
• The etiology and clinical presentation.
• Stable patient with dyspepsia
• An unstable patient with Alarm Features

29. Treatment Options
• Empiric anti-secretory therapy,
• Empiric triple therapy for H pylori infection,
• Endoscopy followed by appropriate therapy based on
findings,
• H pylori serology followed by triple therapy for patients
who are infected.
• Breath testing for active H pylori infection may be used.
• Endoscopy is required to document healing of gastric
ulcers and to rule out gastric cancer.
• This usually is performed 6-8 weeks after the initial
diagnosis of PUD.

30. Endoscopy
Perform endoscopy early in:
• Patients older than 45-50 years
• Patients with alarm symptoms, such as dysphagia,
recurrent vomiting, weight loss, or bleeding.

31. Case
• A 42-year-old man came to follow the result of endoscopy
done few days ago.
Endoscopy Result:
• Antral erosions
• Duodenal erosions
• Urease test is positive for H pylori
• How are you going to manage him?

32. Acid Suppression
Two classes of acid-suppressing medications currently in
use are:
• Histamine-2 receptor antagonists (H2RAs)
• Proton pump inhibitors (PPIs).
• Both classes are available in intravenous and oral
preparations.
• Examples of H2RAs include ranitidine, cimetidine, ....
Examples of PPIs include omeprazole, pantoprazole,
lansoprazole, …..

33. Proton Pump Inhibitors (PPIs)
• Good safety profile
• Adverse effects, especially with long-term and/or high-
dose therapy, such as:
• Clostridium difficile infection,
• community-acquired pneumonia,
• hip fracture,
• and vitamin B12 deficiency.
• PPIs impair gastric secretion of acid; thus, absorption of
any medication that depends on gastric acidity, such as
iron, is impaired with long-term PPI therapy.

34. Triple-therapy regimens for H pylori
A 14-day regimen as shown below:
• Omeprazole: 20 mg PO bid
• or
• Esomeprazole (Nexium): 40 mg PO qd
• Plus
• Clarithromycin: 500 mg PO bid
• and
• Amoxicillin: 1 g PO bid
Alternative triple-therapy regimens
•The alternative triple therapies, also administered for 14 days, are as follows:
• Omeprazole : 20 mg PO bid
• Or
• Esomeprazole (Nexium): 40 mg PO qd
• Plus
• Clarithromycin: 500 mg PO bid
• and
• Metronidazole (Flagyl): 500 mg PO bid

35. A 62-year-old lady, known case of IHD presents with one week
H/O black stools which is documented to be melena on PR.
She was pale and abdomen is soft.
Investigations revealed:
HGB ....................... 96 120 – 160 g/L
PLT .................. .......260 140 – 450 x10.e9/L
What is the most common cause could be responsible for this condition?
Aspirin
The most appropriate next step to do is:
A- Start her on ferrous sulphate
B- Start her on H2 blocker
C- Start her on proton pump inhibitor
D- Refer her for gastroscopy
Answer D

36. Medical Management of NSAID Ulcers
• According to the ACG guideline, all patients who are
beginning long-term NSAID therapy should first be tested
for H pylori.
• NSAIDs should be immediately discontinued in patients
with positive H pylori test results if clinically feasible and
given eradication therapy.
• For patients who must continue with their NSAIDs, PPI
maintenance is recommended to prevent recurrences even
after eradication of H pylori.
• If NSAIDs must be continued, changing to a COX-2
selective inhibitor is an option.

37. Prophylactic or Preventive Therapy
• Patients with NSAID-induced ulcers who require chronic,
daily NSAID therapy
• Patients older than 60 years
• Patients with a history of PUD or a complication such as
gastrointestinal bleeding
• Patients taking concomitant steroids or anticoagulants or
patients with significant comorbid medical illnesses

38. Reference
• American College of Gastroenterology
2012

39. ‫الــوالــديــن‬ ‫بــر‬
THANK
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