This document discusses peptic ulcer disease (PUD), including its definition, epidemiology, etiology, symptoms, investigation, and treatment. PUD is caused by acid and pepsin digestion of the stomach or duodenal lining. Key contributing factors include Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use. Common symptoms are abdominal pain and vomiting. Diagnosis involves endoscopy with biopsy and testing. Treatment aims to relieve symptoms, promote healing, and eradicate H. pylori if present through medications like PPIs, H2 blockers, and antibiotic combinations.

1. PEPTIC ULCER
DISEASE
RICHARD KWAME SERBEH

2. DEFINITION
• The presence of a break in the continuity of gastric or
duodenal mucosa by the action of acid.
• A peptic ulcer is an ulcer caused by the digestion of tissue
by acid/pepsin occurring in areas accessible to acid and
pepsin.
1. The lower end of the oesophagus.
2. Stomach.
3. Duodenum

3. EPIDEMIOLOGY
•PUD is common
•A major source of morbidity and health care expenditure
in Developing countries
•Affects 200.000 - 400.000 people annually
•Accounts for as much as 10% of medical costs for
digestive diseases.

4. •Incidence 0.1%-0.3% per year
•More common with increasing age.
•Previously more common in men than women but
now affects both male and female at similar rates,
•Persons infected with Helicobacter pylori have nearly
a tenfold increase in incidence at 1% per year.

5. AETIOLOGY
•Peptic ulcers occur a result of imbalance between the
offending factors in the GIT and the protective factors of
the GIT
•
OFFENDING FACTORS PROTECTIVE FACTORS
HCL Bicarbonate
H-Pylori Mucous Membrane
Gastrin Prostaglandin
Bile Acid Mucousal Blood Flow
NSAIDS Epithelial renewal

6. AETIOLOGY
It is probably multifactorial and the following factors may be associated.
1. Increased gastric acid secretion from:
(i) Increased stimulus to secretion (a) Neurogenic. (b) Humoral, (c) Food.
(ii) Increased parietal cell mass (a) Genetic. (b) Acquired.
(iii) Failure of inhibition of acid secretion (a) Antral. (b) Duodenal.
2. Impaired defense against acid and pepsin due to:
(i) Incomplete neutralization of acid (a) Inadequate alkali secretion by duodenum,
pancreas or gall bladder. (b) Poor mixing of acid chyme and alkali. _(c) Rapid
gastric emptying.
(ii) Impaired resistance of duodenal mucosa. (a) Ischaemia of mucosal patches
supplied by mucosal end-arteries arising outside the stomach. (b) Reduction in the
protective layer of mucus and glycolipids. (c) Interference with the regenerative
ability of the duodenal epithelium.

7. AETIOLOGY
3. Drugs e.g. non-steroidal anti-inflammatory drugs (NSAIDs),
corticosteroids
4. Colonization by Helicobacter pylori
1. H. pylori is a gram-negative spiral, motile, microaero-philic (requiring lower
levels of oxygen for survival), flagellate, bacterium.
2. It stimulates gastrin release thereby increasing acid secretion.
3. H-pylori also produces a mucinase which destroys the protein structure of
mucus, thereby making defective the mucus barrier of the first few inches of
the duodenum. Evidence of person to person transmission, oral-oral or faecal-
oral

8. • The most common insults/offending factors are:
1. Helicobacter pylori
2. Nonsteroidal anti inflammatory drugs(NSAIDs)
• Uncommon causes of insults include:
Gastric acid hypersecretion(as in Zollinger-Ellision syndrome)
Antral G-cell hyperplasia
Mastocytosis
Viral infections with herpes simplex virus and cytomegalovirus.
Inflammatory disorders e.g.- Chron’s disease or sarcoidosis
Radiation injury

9. Control of Gastric Secretion
• The control of gastric secretion can further be categorized as:
1. Unconditional (presence of food in the mouth)
2. Conditional (food outside the mouth)
• Activities of the GIT is regulated by the enteric nervous system. The
enteric nervous system contains neurons which respond to chemical and
mechanical stimuli. It also secretes NO, noradrenaline, acetylcholine, 5-
HT and many other important peptides

10. Control of Gastric Secretion
• Unconditional Mechanism
(a)Presence of protein in ingested food stimulate G cells of the antrum →
(gastrin)→ECL found at the body and fundus →Histamine→Parietal cells
→ HCL. The produced HCl helps in the conversion of pepsinogen to pepsin
(b) Distension of the stomach wall due the presence of ingested food in the
stomach causes vagal stimulation………
• Conditional Mechanism
• Activation of vagal stimulation at the perception of food

11. HCl Production

12. HCl Production

13. HCl Production

14. HCL Regulation
HCL ↑ HCL↓
Acetylcholine Somatostatin → D Cell →Antrum
Histamin Secretin → S Cell →Jejenum
Gastrin GIP → K Cell →Jejenum/Duodenum
Cholecystokinin → I cell →Duodenum
GIP : Gastric Inhibitory Peptide

15. Important Gastric secretions
• Mucus
• PRotects stomach wall from
corrosive effects of HCL
• Gastrin
• Increases gastric motility
• Relax Pyloric sphincter
• Constricts esophageal sphincter
preventing re-entry
• HCL
• PRovides good PH for enzymatic
reaction
• Eliminates pathgens present in food
and drinks
• Aids in iron absortion
• Helps convert pepsinogen to pepsin

16. Symptoms and Signs
• Vomiting may occur in both duodenal and gastric ulcers
• Abdominal pain
• May be a minor discomfort, gnawing, burning, dull ache or very severe pain
• Typically in the epigastrium or right hypochondrium
• Occasionally high up behind the sternum or low down around the umbilicus
• In duodenal ulcer, typically comes on when the patient is hungry and may wake the
patient up in the middle of the night.
• In gastric ulcer, it is typically worsened by food
• Is relieved by alkalis and food in duodenal ulcer
Sign
Tenderness in the epigastrium, right hypochondrium or umbilical region during an
attack

17. Investigation
• Full Blood count
• Stool Routine Examination
• Oesophago-gastro-duodenoscopy
With biopsy for histology and staining (for H. pylori)
With urease test (for H. pylori)
• Barium meal in the absence of endoscopy

18. Treatment
Treatment objectives
• To relieve pain and reduce gastric acid secretion
• To promote healing of the ulcer
• To eradicate H. pylori if present
• To prevent recurrence of the ulcer
• To avoid complications
Non-pharmacological treatment
• Avoid smoking and alcohol intake
• Avoid foods that aggravate the pain

19. Treatment
Surgery
indications for surgery
• Chronicity - crippling periodic attacks
• Economic factors which make it difficult for the patient to
persevere with medical treatment
• Complications
Perforation
Gastric outlet obstruction
Haemorrhage that does not respond to conservative measures

20. Treatment
Medical Management
H2 receptor blockers
• Cimetidine
• Ranitidine
• Famotidine
Sp. side effects
• Gynecomastia
• imotence
Proton Pump Inhibitors
• Omeprazole
• Esomeprazole
• Rabeprazole
• Pantoprazole
Sp. side effects
• Ca2+↓…..Osteoporosis
• Vit B12↓……Meg Anemia

21. Treatment
Mucus Protective agents
• Sucralfate
• Colloidal Bismuth Subcitrate
Nb: should not be given with
antacids
PGE2 Analogue
• Misoprostol
Nb: contraindicated in Pregnancy
Anticholinergics
• Pirenzepine
• Telenzepine
Antacids
• Alluminium hydroxide
• Magnesium hydroxide

23. Treatment
• H-Pylori eradication