types, etiology, pathogenesis, sign and symptoms

1. PATHOPHYSIOLOGY
PEPTIC ULCERS
Nem Kumar Jain
M.S. (Pharm.) Pharmacology & Toxicology
Assistant Professor
School of Pharmacy
ITM University Gwalior

2. N- nicotinic receptors
M- muscarinic receptors
GRP- gastrin related peptide
Ach- acetyl choline
CCK2 cholecystokinin
Hist- histamine
ECL cell- enterochromaffine
cells
PGE2- Prostaglandin E2
EP3- prostaglandin E
receptor 3
H2- Histamin receptor type 2
PHYSIOLOGY OF GASTRIC ACID SECRETION

3. PEPTIC ULCER
 An Ulcer is …
 Erosion in the mucosal lining of the stomach or the
duodenum.
 Ulcers damage the mucosa of the alimentary tract,
which extends through the muscularis mucosa into the
sub mucosa or deeper.
 Peptic Ulcers are the areas of degeneration and
necrosis of GIT mucosa exposed to acid-peptin
secretion

4. Most Commonly (98-99% cases)
Ulcers that form in the stomach are called Gastric ulcers;
in the duodenum, they are called Duodenal ulcers. Both
types are referred to as Peptic ulcers.
Occurrence Ratio-
Duodenal: Gastric= 4:1
Acute Ulcers (Stress Ulcers)
-Gastric Ulcer
Chronic Ulcers:
- Gastric & Duodenal
More common in males
than in Females (4:1)

5. PEPTIC ULCER

6. ETIO-PATHOGENESIS OF PEPTIC ULCER DISEASE
IMBALANCE:
 Acid
 Pepsin
 Helicobacter pylori
 NSAIDS
 Tobacco
 Smoking
 Psychological Stress
 Hypergastrinemia
(ZES)*
 Spicy food, Coffee
 Prostaglandins
 Mucosal blood flow
 Mucous gel layer
 HCO3
 Epithelial junctions
 Regeneration of the
epithelial layer
 Epidermal growth
factor
AGGRESSIVE FACTORS DEFENSIVE FACTORS
Disruption of Mucosal Lining
Exposure to Gastric acid and pepsin secretion
H. Pylori infection
 * ZES- zollinger ellison syndrom

7. HELICOBACTER PYLORI INDUCED
 1981 - Robin Warren,
M.D., an Australian
pathologist, discovered
numerous bacteria
living in tissue taken
during a stomach
biopsy.
 Spiral urease-
producing, Gram-
negative bacteria
always accompanied
changes in the stomach
lining

8. HELICOBACTER PYLORI
 Gram negative, Spiral bacilli ,Spirochetes
 Do not invade cells – only mucous lining
 Breakdown urea – ammonia and CO2
 Break down mucosal defense: Urease, Protease, catalase,
Phospholipase, Cytotoxin associated gene protein (CagA),
Vacuolating cytotoxin (VacA)
 Chronic Superficial inflammation: Elaboration of IL-1, IL-6,
IL-8, TNF alpha by infected mucus cells
 IL-8 acts as chemoattract for neutrophils and
macrophages---- Acute inflammation (Gastritis)
Test for diagnosing H.pylori
Breath test :by measuring the amount of co2 in exhaled
breath.
Blood test: by identifying H.pylori antibodies by ELISA test.
Stool test :stool sample tested with H.pylori antigen.

9. HOW H. PYLORI SURVIVES THE ACIDITY AND
CAUSE ULCERS

10. NSAID INDUCED ULCERS
 Most commonly used Analgesic and anti-
inflammatory medications: ibuprofen, diclofenac,
aspirin etc.
 Linked to direct toxicity, endothelial damage and
epithelial injury
 NSAIDS Inhibits production of Cytoprotective
Prostaglandins (PGE2 & PGI2) (Inhibits acid
secretion, promotes mucus as well as bicarbonate
ions)
 Disrupt mucosal barrier
 Chronic consumption affects both duodenal and
gastric mucosa.

11. SYMPTOMS
 Food-Pain pattern
 No night Pain
 Nausea or vomiting
 Haematemesis more
common
 Unexplained weight loss
 Anorexia
 Abdominal fullness
 Pain-food-relief pattern
 Pain Starts 2/3 hours after
meals, or in the middle of the
night
 No Vomiting
 Melaena common than
Haematemesis
 Indigestion
 Feeling very hungry 1 to 3
hours after eating
 Mild nausea
Duodenal Ulcers Gastric Ulcers

12. DIAGNOSIS
 Endoscopy:
Flexible tube fitted with
camera is threaded down the
esophagus in to stomach to
see the ulcer by physician
 Barium meal:
Barium liquid is drunk
making ulcer visible on X-ray

13. CONCLUSION

14.  Avoid stress
 Avoid contamination