This document summarizes a seminar on peptic ulcer disease. It defines peptic ulcers, classifies them as acute or chronic, and discusses their etiology, including H. pylori infection and stress factors. It covers the pathogenesis of ulcers, clinical features, diagnosis including tests for H. pylori, and treatment using proton pump inhibitors, H2 receptor antagonists, and antibiotics. It also discusses complications, factors affecting treatment success, adverse drug reactions, drug interactions, and patient counseling.

1. SEMINAR ON PEPTIC ULCER
DISEASE
PRESENTED BY :
WALID S MOMIN
1ST YEAR M.PHARM
DEPARTMENT OF PHARMACY PRACTICE

2. Definition :
 Peptic ulcers are the areas of degeneration
and Necrosis of gastrointestinal mucosa
exposed to acid-peptic secretions.
 The term peptic ulcer describes a condition in
which there is a discontinuity in the entire
thickness of the gastric or duodenal mucosa
that persists in the gastric juice.
 Peptic ulcer is usually represented as

3. CLASSIFICATION OF PEPTIC
ULCERS
 Acute or stress ulcers : Multiple, Small mucosal
erosions.
 Chronic ulcers: Gastric or Duodenal ulcers.

4. ETIOLOGY
 Occurs due to imbalance between the
aggressive and defensive factors.
 Etiological factors of Acute ulcers :
A. Psychological stress
B. Physiological stress
 Shock
 Severe trauma
 Drugs and Local irritants
 Cushing’s syndrome

5.  Chronic ulcer disease : Multifactoral, the main
contributing factor is the H-Pylori infection.
 Acid-pepsin secretions
 Mucus secretion
 Gastritis
 Local Irritants
 Dietary factors
 Psychological factors
 Genetic factors
 Hormonal factors
 Miscellaneous factors

6.  Viral Infections (cytomegalovirus)
 Radiation
 Chemotherapy ( e.g. hepatic artery infusions)
 Idioathic
 Vascular insufficiency
 Cigarette smoking

7. Infection
•H-Pylori Infection
Few months
•Chronic superficial gastritis
Years
•Hyperacidity
Mucosal
layer erosion
•Peptic ulcer

8. MECHANISM OF PEPTIC ACID
SECRETION

9. PATHOGENESIS

12.  H-Pylori contains enzymes like urease, protease,
catalase, phospholipase which damage the mucosal
barrier.
 Basal and Maximal acid output due to various
stimuli.
 Vagal stimulation
Gastric Ulcer : Impaired gastric mucosal defenses
against acid-pepsin secretions.
Pathogenesis : serum gastrin levels due to ingested
food leading to hyperacidity.

13. OTHER SUGGESTED
PATHOGENESIS
 Acid secretion because of parietal cell mass.
 Inhibition of gastric acid secretion.
 Hco3
- secretion in the duodenum due to H-Pylori
infection causing local release of cytokins and
further damage.

14.  NSAIDS induced peptic ulcer :
NSAIDS
COX
inhibition
Adherence
of
leucocytes
to mucosal
endothelial
cells
Decreased
prostagland
in synthesis
Superficial
erosions
Peptic ulcer

15.  A number of other factors may contribute to the
development of NSAID induced mucosal injury,
neurtophils adherence may damage vascular
endothelium and cause reduced mucosal blood flow or
may release oxygen derived free radicals and
proteases.
 Leukotriens have stimulatory effect on neutrophils
adherence.
 Topical irritant properties associated with the acidic
properties of NSAID’s e.g. aspirin and their ability to
decrease hydrophobicity of mucosal gel layer

16. CLINICAL FEATURES
 Epigastric pain
 Upper abdominal pain occurring 1-3 Hrs after meals and
relieved by food or antacids is a classical symptom of
peptic ulcer disease.
 Anorexia, weight loss.
 A typical nocturnal pain that awakens the patient from
sleep.
 Heart burn due to acid regurgitation.
 Nausea may accompany the pain.

17. DIAGNOSIS
 Diagnosis of H-Pylori infection .
 Non-Invasive techniques:
A. Urea breath test
B. Serological tests
C. Stool test
• Invasive techniques
A. Rapid urease test
B. Culture
C. Histology

18.  13C Urea breath test : used to demonstrate eradication
of organism following treatment.

19.  Serological test : used to detect antibodies
 Used in diagnosis and epidemiological studies.
 Stool test : Immunoassay using monoclonal antibodies
for qualitative detection of H-Pylori that leads to colour
change that can be detected visually or by
spectrophotometer.
 Used in the diagnosis and monitoring efficacy of
eradication therapy.
 Culture : Biopsies cultured on a special medium
 Enables sensitivity testing to determine optimum
treatment or antibiotic resistance.
 Histology : Gastric mucosal staining, helps in the

20.  Biopsies are done to exclude malignancy and
uncommon lesions such as crohn’s disease.
 Wireless capsule endoscopy : determines NSAIDS
induced ulceration of small intestine.
 Use of gastrograffin meal:
 Gastrografin (Diatrizoate Meglumine and Diatrizoate
Sodium Solution) is a iodinated radiopaque contrast
medium for oral or rectal administration only.

21.  Rapid urease test :
Gastric biopsies
with urea solution
containing phenol
Urea ammonia
P
H
Rapid colour
change

22. OTHER DIAGNOSTIC TESTS
 Esophagogastroduodenoscpy : permits direct
visualization of superficial erosions and sites of active
bleeding.
 Routine single barium contrast techniques :
 Fasting serum concentration studies :

24. TREATMENT AND
MANAGEMENT
 Non pharmacological therapy :
I. Reduce psychological stress
II. Reduce physical stress
III. Cessation of cigarette smoking
IV. Stop use of NSAIDS
V. Avoid spicy foods, caffeine, alcohol
VI. Drink plenty of water
VII. Avoid fasting and maintain optimum gap between
meals

25. Pharmacological Therapy
 Classification of Drugs:
1. Proton Pump Inhibitors : e.g. omeprazole,
pantaprazole,Lansoprazole.
2. H2receptor antagonists : e.g. Ranitidine, Famotidine,
cimetidine
3. Sucralfate
4. Bismuth compounds
5. Antacids : systemic e.g. Sodium bicarbonate, Non
Systemic e.g. Magnesium Trisilicate.
6. Prostaglandin Analogs : e.g. misoprostol, Enprostil.
 Anti H-Pylori drugs (Antibiotics) e.g. Amoxicillin,
clarythromycin, tetracyclines.

26. Proton Pump
Inhibitors
Carried in
blood stream to
the parietal
cells
Activation
Cytosol ESCInhibition of H+
K+ ATPase
Inhibit acid
secretion

27.  PPI’s differ in their in their potencies.
 Plasma concentration is reached after 2-3 hrs.
 T1/2 48 Hrs.
 To be taken 30 minutes prior to food.
2. H2receptor antagonists :
 Structural analogs of histamine.
 pepsinogen pepsin
 Used in symptomatic treatment.
 Plasma concentration is reached within 1-3Hrs after
administration.
 Recommended in patients with nocturnal gastric acid
secretion and management of dyspepsia symptoms.
( )

28.  Sucralfate : Basic aluminium salt of sulfated sucrose
Polymerizes at pH <
4.0 by cross linking
of molecules
Gel
Adheres to the
ulcer base
Precipitates surface
proteins and acts as
a physical barrier
Antacids are contraindicated when sulfates are
taken

29.  Prostaglandin Analogs :cytoprotective properties
1. Increase mucus and bicarbonate production.
2. Increase mucosal blood flow
3. Inhibit gastrin production
 Antacids : ANC--- No of Meq of 1N Hcl that are
brought to pH 3.5 in 15 minutes by unit dose of
antacid preparation. Mgsio3
Cl- salt
Cl- + HCo3
-
No acid-base
disturbance

30. COMPLICATIONS OF PEPTIC ULCER
DISEASE BLEEDING PEPTIC ULCER :
 Patients with high risk of bleeding are given high dose of
infusion of omeprazole ( 80 mg bolus followed by
8mg/Hr) for 72 Hrs to reduce rebleeding.
 LATE COMPLICATIONS OF PEPTIC ULCER:
 Reactive hypoglycaemia, diarrhoea, weight loss,
anaemia, flushing, plapitation, sweating tachycardia,
postural hypotension.

31.  Treatment :
 Somatostatin analogs for reactive hypoglycaemia.
 Antibiotics
 metachlopramide
 Zollinger-ellison syndrome: use of octreotide, surgical.

32. Recommendations for Treating and Monitoring
Patients with Helicobacter pylori (HP)-Associated and
Nonsteroidal
Anti-inflammatory Drug (NSAID)-Induced Ulcers
 Assess patient allergies
 Assess patient use of alcohol or alcohol-containing
products with metronidazole and oral birth control
medications with antibiotics and counsel appropriately.
 Inform the patient of change in stool color when bismuth
salicylate is included in an HP eradication regimen.
 Assess and monitor patients for potential adverse
effects.
 Assess and monitor patients for potential drug
interactions.
 Monitor patients for salicylate toxicity.

33. o Provide education to patients who are receiving HP
eradication therapy, including why antibiotic and antiulcer
combinations are used, when and how to take medications,
adverse effects, alarm symptoms, when to contact their health
care provider, and the importance of compliance to drug
treatment.
NSAID-induced ulcer
Recommend drug treatment
Assess risk factors for NSAID-induced ulcers and ulcer-related
complications, and when indicated recommend appropriate
strategies for reducing ulcer risk.
Assess and monitor patients for potential drug interactions and
adverse effects (especially misoprostol).

35. FACTORS THAT CONTRIBUTE TO UNSUCCESSFUL
ERADICATION
 Poor Patient compliance
 Resistant organisms
 Increased bacterial load
 Missed dose in a 7 day regimen may also contribute
towards failure of eradication.
 Tolerability
 Preexisting antimicrobial resistance.

36. ADVERSE DRUG REACTIONS
 Proton pump inhibitors :
1. Diarrhea
2. Headache
3. Abdominal pain
4. Nausea and vomiting
5. Microscopic colitis
 H2receptor antagonists :
1. Anti-androgeniceffects gynaecomastia.
2. Impotence

37.  Bismuth chelate:
1. Neurotoxicity
 Sucralfate :
1. Constipation
2. Hypophosphataemia
 Prostaglandin analogs :
1. Diarrhea
2. Abdominal cramps
3. Uterine bleeding
4. Abortion
 Antacids : alkalosis, increase sodium load.

38. DRUG INTERACTIONS
 PPI’s are metabolised by cytochrome p450 isoenzymes,the
affinity of individual proton pump inhibitors for these enzymes
influence the incidence of clinically relevant drug interactions.
 E.g. omeprazole+warfarin warfarin levels.
 benzodiazepines + omeprazole benzodiazepines
levels.
 PPI’s also alter the absorption of other drugs du to altered pH
 E.g. decreased absorption of Ketoconazole
 increased absorption of Digoxin
 Cimetidine interacts with Thiophylline, Diazepam,
Flurazepam, Triazolam.
 All acid suppressing drugs decrease absorption of pH
dependent control release tablets.
 Antacids interact with tetracyclines, ciprofloxacin forming
insoluble complexes or chelates.

39. PATIENT COUNSELING
 Weight loss
 Avoid spicy foods
 Avoid hot beverages
 Maintain optimum time interval between meals
 Reduce psychological stress
 Reduce physical stress
 Cut off irregular eating habits
 Educate the patient about the current principles of
therapeutic management
 Patient should be warned about the specific side effects
to be expected from the regimen and what to do if they
experience any of these side effects.
 Avoid drugs e.g. TCA’s, CCB’s, Anticholinergics,
NSAIDS.

40. References
 Pharmacotherapy by Dipiro
 Clinical Pharmacy and Therapeutics by Roger
Walker
 Pharmacology by K.D Tripati
 Clinical Medicine by Kumar and Clark
 Handbook of Pathology By Harsh Mohan