2. DEFINITION:
PEPTIC ULCER DISEASE (PUD) refers tp group of disease characterized by presence of
ulcers in any portion of GI tract exposed to acid in sufficent duration and concentration.
Commonly occur in
• small intestine ( duodenal ulcers)
•Stomach( gastric ulcers) . It also include barrets ulcer of oesophagus ..
FACTORS CONTRIBUTE TO PUD:
• Hcl, Pepsin.
• H.Pylori
• NSAID’S
• Aspirin
• Gastric Mucosal Ischemia
ETIOLOGY:
H.Pylori( MOST COMMON)
NSAID’S (MOST COMMON)
HYPERSECRETORY CONDITIONS: Zollinger –ellison’s syndrome
MEDICATION: Alcohol, bisphosophonates, corticosteroidsm iron etc.,
Cigarette smoking
INFECTIONS: VIRAL ( CMV, HSV) ; BACT( GI-TB)
3. H.PYLORI – CAUSING ULCERS
Transmission: human human through faeco-oral route
epidemiology: < 10 yrs – uncommon
18-30 yrs – 10%
>60 yrs – 50%
Organism: Spiral shaped ,flagellated urease producing pH sensitive Gram –ve bacteria uses
flagella to burrow through mucosal layer of GIT.
PATHOGENESIS: High duodenal acids promote gastric metaplasia which provide favorable
environment for H.Pylori.
Bacteria enters GIT through
faeco-oral route
Burrows and Enters the GI mucosal
lining
Colonizes and produces
inflammation of mucosa
Increased gastric metaplasia
and increased colonization
Causing ulcers
4. H.Pylori survives in gaatric acid as it converts the gastric acid by urease enzyme to
ammonia and bicarbonate which neutralizes the environment .
NSAID’S:
5. CLINICAL PRESENTATION:
The patient can be asymptomatic or can experience
anorexia
nausea
bloating
heartburn
belching
epigastric pain between xiphoid and umblicus ( hallmark and most frequent symptoms of
duodenal ulcer and gastric ulcers.)
DIAGNOSIS:
•Radiology and Endoscopy : allows direct inspection and visualisations of superficial erosion &
active bleeding site and allows us for taking biopsy samlings.
•Laboratory tests: for h.pylori
rapid urease test
stool antigen test
serology for H.Pylori.
8. ADVERSE DRUG REACTION:
Head ache, diarrhea, abdominal pain , sskin rash , itching.
2. HISTAMINE -2- RECEPTOR ANTAGONISTS:
CIMETIDINE
RANITIDINE
FAMOTIDINE
MOA: (See the diagram) , it supress the gastric acid secretion by reversibly blocking
histamine-2- receptor on surface of gastric parietal cells.
ADR: Nausea, Diarrhea
3.ANTIBIOTICS: CMAT
CLARITHROMYCIN
AMOXICILLIN
METRONIDAZOLE
TETRACYCLINE
Exhibit Anti- Bacterial Effects On H.Pylori
ADR: Rash , dysgeusia, diarrhea, nausea, monolial vaginitis.
9. 4. MUCOSAL PROTECTANT: SUCRALFATE
MOA: It is an non absorbable disaccharide containing sucrose and aluminium. It adheres to base
of ulceration and forms a protective barrier against gastric acids and bile salts.
ADR: Constipation
5. BISMUTH COMPOUNDS: ( BISMUTH SUBSALICYLATE)
MOA: Bismuth penetrates adhesion of H.Pylori to gastric mucosa, decreases resistance when
used with other antibiotics inhibits release of proteolytic enzymes and suppress the growth of
H.Pylori.
ADR: CNS toxicity at high doses , including neurotoxicity, tinnitus , grey black stools.
TREATMENT OF ERADICATION AND RECURRENCE OF PUD:-
PUD treated with Triple Therapy , Quadruple Therapy or Combination Therapy.
Triple therapy: consist of 2 antibiotics and PPI’S for 14 days .
quadruple therapy: consist of bismuth , metronidazole, tetracycline , PPI’S / H2 blockers fo0r
10-14 days.
Combination therapy: bismuth , metronidazole, tetracycline fpr 14 days.
PUD BY NSAID’S: should be treated with antisecretory agents.
PPI’S ,H-2- RECEPTOR ANTAGONIST OR MISOPROSTOL Used to prevent PUD in patients with
chronic NSAID’S and who are at risk of devoloping PUD .