This document summarizes peptic ulcer disease (PUD) and its regulation and management. It defines PUD and ulcers, describing the three pathways that mediate gastric acid secretion - neurocrine, paracrine, and endocrine. It discusses the roles of acetylcholine, histamine, and gastrin in stimulating acid production. Risk factors for PUD include H. pylori infection, NSAID use, smoking, and low socioeconomic status. Symptoms and treatments are also summarized, including triple therapy for H. pylori, antisecretory drugs, bleeding ulcer management, and surgical options.

1. By: Dr. Abhimanyu Prashar

2. PUD:
“A condition in which there is a discontinuity in the
entire thickness of the gastric or duodenal mucosa”
Ulcers:
“The areas of degeneration and necrosis of
gastrointestinal mucosa exposed to acid and pepsin
secretion”

3. Regulation of gastric acid secretion
Mediated by 3 pathways: Neurocrine (Ach)
Paracrine (Histamine)
Endocrine (Gastrin)
• Activation of proton pump exchange of H+
• In addition, histamine, gastrin & ach receptors stimulate H+
production
• Ach from post ganglionic vagal neurons
• Gastrin fron antral G cells stimulates pepsinogen secrection,
hepatic bile flow & pancreas (insulin)

4. It also stimulates gastric & intestinal motility
Directly stimulates Hcl secretion by acting on gastrin
receptors on parietal cells
Gastrin activates ECL cells which releases histamine
Histamine activates H2 rec, results in activation adenylate
cyclase which convers ATP to cAMP and subsequent
generation of H+ & proton pump mobilses & activated

5. Autoregulatory mechanism:
Ingestion of meal gastrin release gastric acid
secretion decreased PH release of somatostatin
from D cells decreased release of gastrin, inhibits
acid secretion, suppress histamine release
Other NTs, vasoactive intestinal peptide, galanine,
serotonin, are also involved in direct or indirect
regulation of gastric acid secretion

7. Epidemiology
PUD is more common in unskilled labourers and low socioeconomic
groups
Smokers and individuals who are on NSAIDs are more prone to
develop PUD
About 10% of the population in developed countries likely to be
affected by PUD
Duodenal ulcer is 4 times more common than gastric ulcer

8. Etiopathogenesis
Infection with Helicobacter pylori
Use of NSAIDs
Local irritants
Dietary factors
Hormonal factors
Decreased mucous secretion

9. H.pylori
A spiral gram negative bacterium
95% of duodenal ulcers & 85% of gastric ulcers are
associated with H.pylori infection
H.Pylori produces Cag A proteins and vacuolating cytotoxins
(Vac A) which activates inflammatory cascade
It expresses sialic acid specific haemagglutinins and a lipid
binding adhesion that mediate binding to the mucosal
surface

10. Enzymes like urease, haemolysins,
neuraminidase and fucosidase involve in
tissue damage
Altered gastrin homeostasis in H.pylori
infection
Hypergastinaemia leads to inflammation and
ulcer formation

12. Use of NSAIDs
NSAIDs cause 3 patterns of mucosal damage
Superficial erosions & haemorrhages
Silent ulcers detected at endoscopy
Ulcers causing clinical symptoms
Mechanism: reduction of mucosal PGs production
Approx. 20% of patients taking NSAIDs experience
Dyspepsia
Approx. 4% of NSAID users suffer from ulcer and ulcer
complications

13. Local irritants
Pyloric antrum & lesser curvature of stomach most
exposed
for longer periods of irritants (like spicy food, alcohol,
tobacco smoking) hence these are common sites for
occurrence of gastric ulcer

14. Dietary
factors
Poor socio-economic status
(malnutrition)
Irregular food habits
Social habits
Consumption of spicy food

15. Hormonal factors
Zollinger-Ellison syndrome (acid secreting
tumours) leads to massive hypersecretion of
gastric acid

16. Decreased mucous secretion
Conditions like stress, anxiety that decreases
quantity
or quality of normal protective mucous barrier
predisposes
to the development of PUD

17. Clinical features

18. Duodenal ulcer
• Pain-food relief pattern
• Night pain common
• No vomiting
• Melena (blood in stool)
more common
• No loss of weight
Gastric ulcer
• Food-pain pattern
• No night pain
• Vomiting present
• Hematemesis (blood in
vomit) more common
• Significant loss of weight

19. Investigations

20. Endoscopy
Radiology

21. H. pylori detection:
Serology to detect
Abs
Urea breath test
Histology & culture

22. Management

23. Triple therapy
Omeprazole 20 mg PO bid
+
Clarithromycin 500 mg PO bid for 7 days
+
Amoxicillin 1 gram PO bid
Omeprazole 20 mg PO bid
+
Clarithromycin 500 mg PO bid for 7
days
+
Metronidazole 400 mg PO tid

24. Quadruple therapy
Bismuth 107.7 mg PO qid
+
Metronidazole 200 mg PO tid
& 400 mg at night
+
Tetracycline 500 mg PO qid
for 14 days
+
Omeprazole 20 mg or
Lansoprazole 30 mg or
Pantoprazole 40 mg PO bid

26. Follow on antisecretory therapy
for complicated ulcers and larger ulcers of ≥ 1 cm
diameter
H2 Rec antagonists
Ranitidine 300 mg PO
or
Nizatidine 300 mg PO
or
Famotidine 40 mg PO
or
Cimetidine 800 mg PO
With evening meal For
additional 4-6 weeks
PPIs
Pantoprazole 40 mg PO
or
Lansoprazole 30 mg PO
or
Omeprazole 20 mg PO
or
Rabeprazole 20 mg PO
For additional 2-4 weeks

27. Bleeding peptic ulcers
Endoscopic haemostasis using a heater probe
or
Inj. Adrenaline 1: 10000 or 1: 100000
Omeprazole 80 mg as a bolus dose then 8 mg/hr
infusion for 3 days

28. Stress ulceration prophylaxis
Ranitidine 300 mg PO 1-0-1
or
Famotidine 40 mg PO 1-0-1
or
Sucralfate 1 gram every 6 hourly
or
Omeprazole 20/40 mg PO 1-0-1
or
Pantoprazole 20/40 mg PO 1-0-1

29. Antacids
Magnesium hydroxide (1g≈ 30 m eq HCl)
Magnesium trisilicate (1g ≈ 10 m eq HCl)
Aluminium hydroxide gel (5 ml ≈ 1 m eq HCl)
Calcium carbonate (1g ≈ 20 m eq HCl)
Sodium bicarbonate (1 g ≈ 12 m eq HCl)
Sodium citrate (1g ≈ 12 m eq HCl)

30. Ulcer protective drugs
Sucralfate (aluminium salt of sulphated
sucrose)
Colloidal bismuth sub citrate

31. Prostaglandin analogues:
Misoprostol (methyl PGE1 ester) 200 mcg
Anticholinergics:
Pirenzepine 100-150 mg/day

32. Drugs causing dyspepsia
Corticosteroids
Bisphosphonates
Potassium chloride
Iron
Antibiotics
CCBs
Nitrates
Theophylline
Drugs with anti muscarinic effects e.g. TCAs
NSAIDs:
High risk: Long acting - piroxicam, ketoprofen
low risk: short acting- ibuprofen, diclofenac
reduced risk: highly selective COX-2 inhibitors

33. ZES
Characterized by severe peptic ulceration,
gastric acid hyper secretion and a non β-cell
islet tumor of the pancreas (gastrinoma)
ZES is the cause of about 0.1 % of cases of
duodenal ulceration

34. Gastrinoma
Secretes
Large amount of gastrin
Stimulates
Parietal cells
Maximal acid secretion & increased parietal cell mass
Increased acid output
Reduced luminal PH to 2 or less
Inactivate pancreatic lipase & precipitates bile acids
Diarrhea & steatorrhoea
Pathogenesis

35. Clinical features:
Diarhoea & Steatorrhoea
Investigations:
serum gastrin levels
Endoscopic ultrasound

36. Management
Non-pharmacological:
Tumor resection
Pharmacological:
Omeprazole 60-80 mg/D
Synthetic somatostatin analogue:
Octreotide SC 200-300 mcg/D BD