Pathophysiology of peptic ulcer. including gastric and duodenal ulcers.

1. Peptic Ulcer Disease
SWALIHA C K
Assistant Professor
Sengundhar College of Pharmacy

2. OUTLINE
• Introduction
• Etiology/ Risk factors
• Types of PUD
• Clinical Presentation
• Pathophysiology
• Investigation/ Diagnostic test
• Complications of PUD
• Management

3. INTRODUCTION
• Peptic Ulcer is a lesion in the lining
(mucosa) of the digestive tract, typically
in the stomach or duodenum, caused by the
digestive action of pepsin and stomach
acid.

4. •Lesion may subsequently occur into the lamina propria
and submucosa to cause bleeding.
•Most of peptic ulcer occur either in the duodenum, or in
the stomach – Ulcer may also occur in the lower
esophagus due to reflexing of gastric content – Rarely in
certain areas of the small intestine

5.  Serious medical problem
 Approx. 500,000 new cases each year
 5M people affected in USA only
 Mostly occur between 55 ot 65 years of age
 Duodenal ulcer more common in men than women
 Gastric ulcer more common in women than men
EPIDEMIOLOGY

6.  Duodenal ulcers are four times more common
than gastric ulcers
 Mortality rates from peptic ulcer are low
 High prevalence
 One of several upper GIT diseases that is caused
,partially, by gastric acid
 Wide range of symptoms

7. ETIOLOGY
• Lifestyle
– Smoking
– Acidic drinks
– Medications
•
•
H. Pylori infection
– 90% have this bacterium
– Passed from person to
person (fecal-oral route
or oral-oral route)
Age
– Duodenal 30-40
– Gastric over 50
•
•
Gender
– Duodenal: are increasing
in older women
Genetic factors
Other factors: stress can
worsen but not the cause

8. RISK FACTORS
 Alcoholic cirrhosis
 Smoking or chewing
tobacco
 Serious illness
 Radiation treatment of
the area
 H-pylori infection
 NSAID’s
 Psychological stress
 Viral infections

9. TYPES
• GASTRIC PEPTIC ULCER
• DUODENAL PEPTIC ULCER

10. Gastric and Duodenal Ulcers

11. CLINICAL
PRESENTATION

12. • Abdominal pain
• Located in epigastric area
• Burning in quality
• Occur on an empty stomach 2-4 hours
after meal or at night (nocturnal pain)
• Relieved by antacids
SYMPTOMS

13.  Perforations
 Blotting and abdominal fullness
 Nausea and vomiting
 Loss of appetite (because of pain)
 Weight loss
 Stomach obstruction
 Heartburn
 Hematemesis
 Melena
 Deep tenderness

14. PATHOPHYSIOLOGY

15. •Under normal conditions, a physiologic balance
exists between gastric acid secretion and
gastroduodenal mucosal defense.
•Mucosal injury and, thus, peptic ulcer occur
when the balance between the aggressive factors
and the defensive mechanisms is disrupted.

16. Aggressive factors, such as NSAIDs, H pylori
infection, alcohol, bile salts, acid, and pepsin, can
alter the mucosal defense by allowing back
diffusion of hydrogen ions and subsequent
epithelial cell injury

22. INVESTIGATION/
DIAGNOSTIC TEST

23. INVESTIGATION
• Stool examination for fecal occult blood.
• blood count (CBC) for decrease in blood
cells.

24. DIAGNOSTIC TEST
• Esophagogastrodeuodenoscopy (EGD)
– Endoscopic procedure
– Upper gastrointestinal series (UGI)
– Urea Breath Testing

25. In all patients with “Alarming symptoms” endoscopy
is required.
Dysphagia.
Weight loss.
Vomiting.
Anorexia.
Hematemesis or Melena

26. Complications of Peptic Ulcers
Hemorrhage
– Blood vessels damaged as ulcer erodes into the muscles of stomach or
duodenal wall
Perforation
– An ulcer can erode through the entire wall
– Bacteria and partially digested food spill into
peritoneum =peritonitis
Narrowing and obstruction (pyloric)
– Swelling and scarring can cause obstruction of food leaving
stomach=repeated vomiting

27. MANAGEMENT
• LIFE STYLE MODIFICATION
• HYPOSECRETORY DRUG THERAPY
• H. pylori ERADICATION THERAPY
• SURGERY

29. THERAPEUTIC AGENTS
Proton Pump Inhibitors
Suppress acid production
•Pantoprazole, rabeprazole
H2-ReceptorAntagonists
– Block histamine-stimulated gastric secretions
– Cimetidine, ranitidine

30. Prostaglandin Analogs
– Reduce gastric acid and enhances mucosal resistance to
injury
– Misoprostol
Mucosal barrier fortifiers
– Forms a protective coat
• Carafate/Sucralfate
– cytoprotective
Antacids
• Neutralizes acid and prevents formation of pepsin
[Al(OH)3, Mg(OH)2] - (Maalox, Mylanta)
• Give 2 hours after meals and at bedtime

31. H. pylori Eradication Therapy:

32. Indications:
Failure of medical treatment.
Development of complications
High level of gastric secretion and
combined duodenal and gastric ulcer.
Principle:
Reduce acid and pepsin
secretion.

33. Types of Surgical Procedures
GASTROENTEROSTOMY
Creates a passage between the body
of stomach to small intestines.
• Allows regurgitation of alkaline
duodenal contents into the
stomach.

34. Types of Surgical Procedures
• VAGOTOMY
– Cuts vagus nerve
– Eliminates acid-
secretion stimulus

35. Types of Surgical Procedures
• PYLOROPLASTY
Widens the pylorus to
guarantee stomach
emptying even without
vagus nerve stimulation

36. THANK YOU