1. PUD Diagnosis & managementBy
Prof. KHALED HEMIDA
Ain Shams University

2. Objectives Definition of peptic ulcer
Comparison of duodenal & gastric ulcers
Etiology
Clinical presentation
Management

3. A break in superficial epithelial cells penetrating down
What is a peptic ulcer?
A break in superficial epithelial cells penetrating down
to muscularis mucosa

4. Definition 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)

5. Imbalance between Protective factors Aggresssive factors
Mucous production Bicarbonate secretion Prostaglandins Mucosal blood flow High epithelial cell turnover
Gastric acid
Proteolytic enzyme
NSAIDS
Bile acids
H Pylori
Alcohol
Pancreatic enzymes
Cigarette smoking
Corticosteroid use

6. Pathogenesis

7. Peptic Ulcers: Gastric & Dudodenal

8. Etiology Old New No acid no ulcer Idiopathic Stress Smoking Spicy food
No H.Pylori no ulcer
NSAIDs
Crohn`s disease
Gastrinoma
Hyperparathyroidism

9. Etiology H. pylori infection NSAID use Cigarette smoking
70-90% of gastric ulcers
80-90% of duodenal ulcers
NSAID use
Cigarette smoking
Increased risk of developing ulcers
Impairs healing
Increases incidence of recurrence
Family history
May reflect genetic susceptibility or intrafamilial

10. H. Pylori Urease producing, gram negative bacillus
Developing countries
Infection increases with age
Infects mucosa of stomach > inflammatory response >
gastritis > increased gastrin secretion > gastric
metaplasia > damage to mucosa > ulceration
Increased risk of developing gastric adenocarcinoma

11. Helicobacter pylori: No acid No ulcer No HP No ulcer
Most common infection in the world (20%)
10% of men, 4% women develop PUD
Positive in % of PUD patients.
H.pylori related disorders:
Chronic gastritis – 90%
Peptic ulcer disease – %
Gastric carcinoma – 70%
Gastric lymphoma
GERD .
Non ulcer dyspepsia
No acid
No ulcer
OLD TESTAMENT
No HP
No ulcer
NEW TESTAMENT

12. H.Pylori & PU Acid hyper secretion in DU Acid hypo secretion GU
Acid normal secretion in normal PH positive
population

14. H Pylori infection

16. Clinical Diagnosis

17. GU Versus DU GU DU Hunger pain Postbrandial pain No vomiting Vomiting
Melina > hematemesis
Good appetite
Eats almost anything
No weight loss
H. pylori infection common,up to 95%
First part of duodenum – anterior wall
Male to female ratio—4:1
More common in patients with blood group O
Postbrandial pain
Vomiting
Hematemesis > melina
Afraid to eat
Lives on milk & fish
Loses weight
Less related to H. pylori than duodenal ulcers : about 80%
Lesser curvature of stomach
Male to female ratio—2:1
More common in patients with blood group A

18. Diagnosis of HP Non endoscopic Endoscopic HP serology
Urea breath test
HP Antigen in stool
HP Ag in saliva
Rapid ureas test (Clotest)
Gastric biopsy & histology
Culture
PCR

19. Indications Noninvasive Testing for H. pylori
Strongly Recommended
Advisable
Dyspepsia
History of/active PUD
Gastric MALT lymphoma
Following gastric cancer
resection
Following peptic ulcer surgery
First-degree relative with
gastric cancer
Long-term (NSAID) therapy
Family history of
duodenal ulcer
Family members with
H. pylori infection
GERD requiring long-term
PPI therapy
1. Malfertheiner P, et al. Aliment Pharmacol Ther. 2002;16:167. 2

20. Tests for H.Pylori Infection
Non endoscopic
Advantage
Disadvantage
Serologic Tests
Detect IgG or IgA
Widely availabe,
least expensive
+ve results reflects reflect
infection , not recommended for confirming eradication,Less sensitive and specific
(90-100% and 76-96%)
Inaccurate tests are common in
elderly, & cirrhotics
Not useful for follow-up
High -ve & +ve predictive values. Sensitivity and specificity
(88-95% and %)
Usefull before & after 4-6 weeks treatment.
Reliable in kids >6 yrs
Best test in elderly population
Most reliable non-endoscopic test to document eradication after treatment
False –ve results presence in
the of PPIs or with recent use of antibiotics or bismuth preparations.pt should be offthese medications at least 2-4 weeks
Urea breath test
False positive (decreased specificity)
in Patients with acute UGI bleed
False negative tests (decreased sensitivity) :
- if patient is on PPI in prior 2 ws
- has taken antibiotics in prior 4 ws
- (24 hours for H2 blocker)
Sensitivity and specificity ~90%
With monoclonal antibody test
Useful before & 4-8 weeks
after treatment
Faecal Antigen test

21. Tests for H Pylori Infection
Endoscopic
Advantage
Disadvantage
Urease- based test
Clotest
Rapid ,inexpensive & accurate
Sensitivity: 90-95% but specificity is %.
False –ve results possible in the presence of PPIs or with recent use of antibiotics or bismuth preparations
So neg. urease test in patients taking these above drugs
does not rule out H pylori
Histologic assessment
Good sensitivity & specificity
Requires trained personnel
Excellent specificity, provides opportunity to test for antibiotic sensitivity
Variable sensitivity requires traine staff and properly equipped facilities
Culture

22. Complications of PU Bleeding : anemia , hematemesis ,melina
Obstruction:
vomiting , dysphagia ,weight loss
Perforation:
Pain ,peritonitis
Carcinoma :
in chronic gastric ulcer

23. Management
Life style modifications
Drug treatment
Surgery

24. Treatment Life style & Dietary Modifications: - Less tress
- Regular diet
- Avoid NSAIDs
- Quit smoking

25. Drugs Gastric acid neutralizers Antisecretory drugs Cytoprotectives
HP eradication

26. Gastric acid neutralizers-Anatacids
The first & historically most widely used drugs
Inhibits the conversion of pepsinogen to pepsin
Fast onset of symptom relief
Frequent dose-7 times per day

27. Anti-secretory Drugs

28. Release of Gastric Acid

29. Anti-secretory Drugs H2RA’s PPI’s Cimetidine - Ranitidine
Famotidine - Nizatidine
Only target 1 of 3 pathways
that eventually act on the
proton pump
More effective during fasting
and sleep
Can develop tolerance
Omeprazole - Lansoprazole
Rabeprazole - Esomeprazole
Pantoprazole
Targets the proton pump
itself
More effective for meal-
related acid secretion
No tolerance issues
More effectively keeps gastric
pH >4

30. Cytoprotectives Sucralfate: ( alumnum hydroxide+ sucrose)
Form a past to protect GI mucosa
1 gm QID

31. HP eradication

32. Indications for eradication of HP
Strongly recommended
Treatment advised
DU & GU
MALT lymphoma
Atrophic gastritis
Recent resection of
gastric cancer
Functional dyspepsia
GERD (patients requiring long-term acid suppressive therapy)
Use of NSAIDs
Maastricht Consensus Report

33. Practical options for HP eradication in Autralia
First & second line therapies
7 days
PPIs standard dose BD+Clarythromycin 500 md+ Amoxill 1 gm (BD)
7 days
PPIs standard dose BD+ Clarythromycin 500 mg+ Metronidazole 500 mg(BD)
14 days
PPIs standard dose BD+ Colloid bismuth subsitrate 120 mg qid +Tetracyclin 500 qid mg + Metronidazole 400 mg qid
10 days
PPIs standard dose BD+ Amoxycillin 1000 mg BD For 5 days
Followed
by 5 days Clarythromycin 500 mg BD+ Tinidazole 500 mg BD
Second line (rescue/salvage) therapy
14 days
PPIs standard dose BD+ Colloid bismuth subsitrate 120 mg qid + furazolidone 200 mg BD +Tetracyclin 500 qid mg
14 days
PPIs standard dose BD+ Amoxill 1 gm (BD)+ rifabutin 150 mg + ciprofloxacin 500 mg BD

34. Duration of Treatment Course of 7-14 days
7-day course more common in Europe
10-14-day course recommended in US
Triple therapy: days
Quadruple therapy: days

35. New Regimens Trial of quadruple therapy for non-responsive cases
(ie, salvage)
Regimens with levofloxacin instead of clarithromycin
Sequential therapy
5 days of one regimen (PPI + amoxicillin) followed by 5
days of a second regimen (PPI, clarithromycin,
tinidazole)
Lactoferrin and Probiotics

36. Continued Acid Suppression
Can discontinue PPI after 4 weeks in uncomplicated ulcers
But maintenance acid suppression may be warranted (even
after H pylori eradication) in complicated ulcers since cure
does not mean elimination of complications
Once daily dose of PPI effective
Maintains pH >3

37. Re-infection of HP
Re-infection following successful bacterial cure is unusual
Commonly represents recrudescence of the original bacterial strain
In adults, reacquisition of the bacteria occurs in
<2%/persons/year which is similar to the rate of
primary infection in adults

38. Re-infection of HP Re-infection rate 7.6%-23.5% 58.8% same strain
Recurrent ulcer in re-infected group 22-25%
Not related to age , sex, ulcer location or eradication
regimens

39. Resistance to eradication
Resistance to clarithromycin 7.8%
Resistance to amoxicillin 0%
Resistance to Metronidazole 39.2%
Clarithromycin-based therapy still the first choice
with eradication rate of 92.6%
Ga,Xia HH., Digestion 2006

40. Risk factors for resistance
Metronidazole resistance
Clarithromycin resistance
- Sex :
female > male
- Ethnicity :
Asian >European
- Test method :
use of E test vs.
agar dilution
- Geographical region :
prescribing
trends/genotype
- Age :
increasing age
-Sex :
female >male
- Ulcer status :
inactive >active

41. NSAID and H. pylori eradication
H. pylori eradication is of value in chronic NSAID users
but is insufficient to prevent NSAID related ulcer disease
completely
In naive NSAID users H. pylori eradication may prevent
peptic ulcer and bleeding
For patients with a history of an ulcer complication who
require subsequent therapy with an NSAID or aspirin, PPI
maintenance treatment is better than H. pylori eradication
in preventing ulcer recurrence and/or bleeding.
Co-therapy may be an option
Patients taking long term aspirin and who bleed should
be tested for H. pylori, & be treated if positive.

42. Risk factors for NSAIDs complications
Prior history of GI ulcer or hemorrahge
Age > 60 yrs
High dosage of NSAID
Concurrent use of corticosteroids
Concurrent use of anticoagulants

44. Testing to prove H. pylori eradication
The ACG guidelines include four groups for post-treatment
testing to confirm eradication:
Patients with H. pylori associated ulcers
Patients who have undergone resection of early gastric
cancer
Patients with H. pylori associated MALT lymphoma
Patients with dyspeptic symptoms persisting after the test
and treat strategy

45. Indications of Surgery in PU
A. Refractory ulcer
B. Complications :
1. Bleeding
2. Perforation
3. Pyloric stenosis

46. Thanks
2004