A short description of peptic ulcer disease along with ayurvedic description.

1. Peptic Ulcer Disease
Presenter-
Dr. Twinkle Joshi

2. Introduction
• Peptic ulcer disease (PUD) refers to ulceration of the mucosa
anywhere in the GI tract exposed to acid and pepsin.
• Ulcers : breaks in the mucosal surface >5 mm, with depth to the
sub-mucosa.
• They can range in size from a few millimeters to a few centimeters
• The 2 most common forms/locations of PUD are
– Duodenal ulcer
– Gastric ulcer
 Site
• Lower esophagus
• Stomach
• Duodenum

3. Types
Acute
• Superficial erosion
• Minimal erosion
Chronic
• Muscular wall erosion with formation of fibrous tissue
• Present continuously for many months or intermittently

4. Aggressive factors
Hydrochloric acid and
pepsin
destroy gastric and duodenal
mucosa.
Defensive factors
Mucus and bicarbonate
ion secretions
protect mucosa Na
bicarbonate is considered as a
buffer so it inhibits auto
digestion of the stomach wall
Prostaglandins (PGE2 &
PGI2)
protect
mucosa
by
inhibiting acid
secretion
increasing mucus and
bicarbonate production
enhancing mucosal
blood flow.
• Imbalance between aggressive factors (acid &pepsin) and defensive factors (e.g. prostaglandins, mucus &
bicarbonate layer).
• However, nowadays, it seems that H. pylori is a major cause
Pathophysiology
One of the main action of
Prostaglandins is increase the
turnover and regeneration of damaged
cells

5. Diffusion of Acid

7. Etiology
• Common causes of PUD
– Helicobacter pylori (H.pylori) infection
– Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
– Critical illness (stress-related mucosal damage)
• Uncommon causes of PUD
– Idiopathic (non-H.pylori, non- NSAID)
– Hypersecretion of gastric acid (e.g. Zollinger Ellison
syndrome)
– Viral infections
– Radiation therapy
– Chemotherapy

8. • Helicobacter pylori (HP) is a spiral shaped,
gram negative, flagellated bacteria first
associated with PUD in the early 1980’s
• Found in most people with duodenal and
gastric ulcers
– About 95% of those with duodenal ulcers
– About 80% of those with gastric ulcers
• HP is primarily spread through the fecal to
oral route
• People are most often infected during
Helicobacter pylori

9. • Mechanisms by which HP causes mucosal
injury are not entirely clear but occurs
through a combination of the following
mechanisms:
– HP catalyzes urea  ammonia is produced 
ammonia erodes the mucous barrier and
causes epithelial damage
– HP produces cytotoxins
– HP produces mucolytic enzymes

10. NSAIDs
• In long-term NSAID users, there is a 10% -
20% prevalence of gastric ulcers and a 2%
- 5% prevalence of duodenal ulcers
• Mechanisms for NSAID-induced ulceration
– NSAIDs are weak acids and are non-ionized
at gastric pH
• Diffuse freely across the mucous barrier
into gastric epithelial cells  H+ ions are
liberated and cause cellular damage
• Aspirin is the most ulcerno-genic of all NSAIDs.

11. • NSAIDs inhibit cyclooxygenase activity
and therefore decrease prostaglandin
production which results in a:
• Reduction in gastric and mucosal blood
flow
• Decrease in mucous and bicarbonate
secretion
• Decrease in cellular repair and
replication
– Greater than 60 years old
– With a prior history of PUD

12. Zollinger Ellison Syndrome
• ZES is characterized by gastric acid hypersecretion and
recurrent peptic ulcers that result from a gastrin-
producing tumor
– More than 50% of gastrinomas are malignant
• ZES is suspected for patients with multiple ulcers and
recurrent or refractory PUD often accompanied by
esophagitis or ulcer complications
• Only accounts for 0.1% to 1% of those with duodenal
ulcer

13. Other factors
• Cigarette smoking
– Impairs ulcer healing and increases the risk of
recurrence
• Psychological stress
– Stress may induce behavioral risks such as smoking
and the use of NSAIDs or may alter the inflammatory
response or resistance to HP infection
• Dietary factors
– Certain foods (e.g. coffee, tea, carbonated beverages,
beer, milk, spices) may cause dyspepsia but do not
increase the risk of developing PUD

14. Signs and symptoms
• Symptoms depend on ulcer location, ulcer
etiology, and patient age
• Many patients, particularly the elderly, have few
or even no symptoms
• NSAID-induced ulcers are often silent
– Complications such as bleeding and
perforation are often the initial presentation

15. • Pain localized to the epigastrium is the most common
symptom
• The pain is described as burning, gnawing, cramping, or
hunger
• A typical nocturnal pain that wakes the patient from
sleep (especially between 12 and 3am)
• The severity of ulcer pain varies from patient to patient
and may be seasonal, occurring more often in the spring
or fall

16. • Episodes of pain usually occur in clusters,
lasting up to a few weeks followed by a pain-free
period or remission lasting weeks to years
• Changes in the character of pain may suggest
the presence of complications
• Pyrosis (heartburn), belching, and bloating may
accompany the pain

18. Gastric Ulcers
• Less common than duodenal ulcers
– Especially in chronic NSAID use
• Most commonly located in the lesser curvature of the
antrum of the stomach
• More common in people greater than 60 years old
Characterized by
• A normal to low secretion of gastric acid
• Back diffusion of acid is greater (chronic )
• Critical pathologic process is amount of acid able to penetrate mucosal barrier
• H pylori is present in 50% to 70%
• Drugs --- Aspirin, corticosteroids, N SAIDs, reserpine, Chronic alcohol abuse,
chronic gastritis

19. Duodenal Ulcers
• Most common form of PUD
– It is 3 times more common than gastric ulcers
• Usually located in the duodenal bulb of the small
intestine
• Most commonly occurs in people between the
ages of 30 and 50
• Associated with ↑HCl acid secretion
• H.pylori associated in 9 0- 9 5 % of cases
• Diseases with ↑risk of duodenal ulcers
COPD, cirrhosis of liver, chronic pancreatitis,
hyperparathyroidism, chronic renal failure

20. Complications
• 3 major complications
Hemorrhage - 15% of patients with active PUD
Perforation - 7% of patients with active PUD
Gastric outlet obstruction
• Initially treated conservatively
• May require surgery at any time during course of
therapy

21. Diagnostic Studies
• Endoscopy procedure
– Determines degree of ulcer healing after treatment
– Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer
• Tests for H.pylori
– Noninvasive tests
• Serum or whole blood antibody tests
– Immunoglobin G (I g G)
• Urea breath test
• C 14 breath test
• Fecal antigen test
– Invasive tests
• Biopsy of stomach
• Rapid urease test

22. Rapid Urease Testing
– Rapid urease tests detect the presence of ammonia in the
biopsy sample
– The ammonia is generated by H.pylori urease activity
– Test of choice at endoscopy
– Greater than 90% sensitive and specific
– Easily performed with rapid results
– Tests for active HP infection

23. Urea Breath Test
• Detects the exhalation of radioactive CO2
following ingestion of 13C or 14C radiolabeled
urea
• H. pylori hydrolysis of the radiolabeled urea
results in radiolabeled CO2 production
• 97% sensitivity and 95% specificity

24. Fecal Antigen Test
• Polyclonal antibody test that detects the
presence of H.pylori antigen in the stool
• Sensitivity and specificity similar to urea breath
test
• Patients may have a reluctance to collect stool
samples

25. • The urea breath and fecal antigen tests may be
falsely negative in patients who have recently
taken
– Antibiotics (up to 4 weeks)
– Bismuth compounds (up to 4 weeks)
– Antisecretory agents (up to 2 weeks)

26. • Barium contrast studies
– Widely used
• X- ray studies
– Ineffective in differentiating a peptic ulcer from a
malignant tumor

27. Treatment
Medical regimen consists of
– Adequate rest
– Dietary modification
– Drug therapy
– Elimination of smoking
– Long-term follow-up care
Aim of treatment program
– ↓ degree of gastric acidity
– Enhance mucosal defense mechanisms
– Minimize harmful effects on mucosa

28. Drug Therapy
• Antacids
• H2 receptor blockers
• PPIs
• Antibiotics
• Anticholinergics
• Cytoprotective therapy

29. Histamine receptor blocks (H2 R blockers)-
famotidine,cimetidine
Used to manage peptic ulcer disease
Block action of histamine on H2 receptors
↓ HCl acid secretion
↓ conversion of pepsinogen to pepsin
↑ ulcer healing
Proton pump inhibitors – pantoprazole, rabeprazole
– Block ATPase enzyme that is important for secretion of HCl acid
Antibiotic therapy
– Eradicate H. pylori infection
– No single agents have been effective in eliminating H. pylori

30. • Antacids – calcium carbinate, MgOH
– Used as adjunct therapy for peptic ulcer disease
– ↑ gastric pH by neutralizing acid
• Anticholinergic drugs- Dicyclomine
– Occasionally ordered for treatment
– ↓ cholinergic stimulation of HCl acid
• Bismuth preparations
• Agents
– Bismuth subsalicylate
– Bismuth exhibits antimicrobial activity against bacterial and viral
gastrointestinal pathogens

31. • Standard triple therapy regimen contains
– Amoxicillin 1000mg twice day + Clarithromycin 500mg twice a day + a
PPI dosed once to twice a day
– Given for 10 to 14 days
• 14 day regimens are generally preferred as 14 day regimens
significantly increases the eradication rate
• Bismuth-based quadruple-therapy contains
– Tetracycline 500mg 4 times day +Metronidazole 250-500mg 4 times a
day + Bismuth subsalicylate 525mg 4 times a day + a PPI once or twice
a day OR H2-receptor antagonist twice a day

32. Refractory Ulcers
• When symptoms, ulcers, or both persist beyond 8 to 12 weeks
despite conventional treatment as previously described or
when several courses of H. pylori eradication therapy fail
• Patient should undergo an upper endoscopy to assess the
situation
• Treatment depends on cause and may include additional H.
pylori eradication attempts, higher PPI dosages, or surgery

33. Nutritional therapy
• Dietary modifications may be necessary so that foods and
beverages irritating to patient can be avoided or eliminated
• Nonirritating or bland diet consisting of 6 small meals a day
during symptomatic phase
• Protein considered best neutralizing food
– Stimulates gastric secretions
• Carbohydrates and fats are least stimulating to HCl acid
secretion
– Do not neutralize well

34. Surgical Treatment
• < 20% of patients with ulcers need surgical
intervention
• Indications for surgical interventions
Intractability
History of hemorrhage, ↑ risk of bleeding
Prepyloric or pyloric ulcers
Multiple ulcer sites
Drug-induced ulcers
Possible existence of a malignant ulcer
Obstruction

35. Surgical procedures
 Gastroduodenostomy
 Gastrojejunostomy
 Vagotomy
 Pyloroplasty

36. A. Billroth I Procedure B. Billroth II Procedure

37. Thank you