This ppt is suitable for b.pharma students. This ppt is prepared according to b.pharma IInd semester syallbus. In this ppt we provide all topics related to pathophysiology of peptic ulcer. In this ppt we covered introduction, types, sign & symptoms, pathophysiology, diagnosis, complications and treatments.

1. PATHOPHYSIOLOGY OF
PEPTIC ULCER
Rajat Srivastava
Assistant Professor
ARK College of Pharmacy,
Kaushambi, UP

2. INTRODUCTION
 Peptic ulcer also known as peptic ulcer disease.
 A condition in which there is a discontinuity in the
entire thickness of the gastric or duodenal mucosa that
persists as a result of acid and pepsin in the gastric
juice.
 The term peptic ulcer applies to mucosal ulceration
near the acid bearing regions of GIT.

3.  A condition in which wounds appear in the lining
of stomach or duodenum, along with a burning
stomach pain is termed peptic ulcer.
 In this case, a low pH peptic juice (acid) secreted
by the walls of stomach or duodenum starts
eroding the mucosa.
 Peptic ulcer disease (PUD) = Mucosal defect in the
GIT (gastric or duodenal) exposed to acid and pepsin
secretion.

4. Sites of peptic ulcer
 Duodenum…………………….80%
 Stomach………………………..19%
 Duodenum & Stomach………..4%

5. Peptic Ulcer

6. Types: Peptic ulcer are mainly of following
of two types-
 Gastric ulcers: This ulcer type affect the stomach
lining and may be acute or chronic. It is
characterized by pain while the food is still in the
stomach.
 Duodenum ulcers: This ulcer type affect the
upper part of small intestine and may acute or
chronic. It is characterized by pain when
stomach is empty, or may result after several
hours of food consumption.

7.  Epigastric pain occurring 30
minutes to 1 hour after
meals
 Aggravated by eating
(because acid secretion
increase at meal time) leads
to weight loss.
 Relieved by vomiting
(because acid is expelled
out).
 No pain at hours of sleep
(HCL production decrease at
hours of sleep).
 More common in person
older than age 50.
 Epigastric pain occurring 2-3
hours after meals.
 Relieved by food (because
the pyloric sphincter, at the
junction of stomach and
duodenum, closes upon
eating to concentrate food in
the stomach) causes weight
gain.
 Not relived.
 Pain at hours of sleep
(because gastric emptying
continuous at hours of
sleep).
 More common between age
25 and 50.
Gastric ulcer Duodenum ulcer

8. ETIOLOGY/CAUSES OF PEPTIC ULCER
 Helicobacter pylori, Gram –ve microaerophillic
bacterium found in gastric antrum of human
stomach. 95% duodenum ulcer & 80% gastric
ulcer associated with H.Pylori.
 NSAID’S like aspirin, ibuprofen, etc. used
frequently.
 Alcoholism
 Smoking
 Radiotherapy
 Cancer of stomach

9. PATHOPHYSIOLOGY
 Pepsinogen is activated to pepsin in
presence of HCl and a pH of 2 to 3.
 Secretion of HCl by parietal cells has a pH of
0.8.
 pH reaches 2 to 3 after mixing with
stomach contents.
 Surface mucosa of stomach is renewed about
every 3 days.
 Mucosa can continually repair itself except
in extreme instances.

10.  Mucosal barrier prevents back diffusion of acid
from gastric lumen through mucosal layers to
underlying tissue.
 Mucosal barrier can be impaired and back
diffusion can occur.
 HCL freely enters mucosa when barrier is
broken
 Result:
 Injury to tissue occurs
 cellular destruction and inflammation

11. BACK DIFFUSION OF ACID

12. H.PYLORI INDUCED ULCER
Gram negative bacteria produced heat shock proteins
Cytokines, histamine, lipopolysaccharides, certain enzymes
Phospholipase
Urease, protease, etc.
•Urease convert in acidic media urea into
ammonia and carbon dioxide. Ammonia itself
cause destruction of mucosal lining.

13.  Ammonia cause infection of mucosal lining and
ultimately inflammatory mediators release.
 Cytokines, leukocytes adhesion and
inflammatory reactions starts
Damage mucosa of GIT
Ulcer occurs

14. DRUG INDUCED ULCER
 Approximately 15% of patients on long-term
NSAID develop PUD.
 NSAIDs - ↓prostaglandin (PG) by inhibiting the
cyclooxygenase (COX) enzymes.
 Three iso-enzymes COX-1, COX-2, COX-3
 COX-1 → PG production in gastric mucosa.

15. Arachidonic acid
Prostaglandins
Controls gastric juice secretions
Damage mucosal lining lead to ulcer
COX-1 & COX-2

16. STRESS INDUCED ULCER
In stress energy consumption increase so
increase glycolysis which is usually done by
cortisol hormone
This hormone inhibit phospholipase A2
No arachidonic acid formation no
prostaglandin increase gastric juice
secretions
Cause ulcer

17. STEROIDS INDUCED ULCER
Steroids acts
on cell
membrane
(Phospholipid)
Inhibit
phospholipase
Inhibits
arachidonic
acid no
prostaglandins
and damaging
of mucosal
lining cause
ulcer

18. SIGNS & SYMPTOMS
Abdominal pain
Nausea
Vomiting
Weight loss
Fatigue
Heartburn
Indigestion
Chest pain
Blood in vomiting
Bloody or dark tarry stools
Loss of appetite

19. COMPLICATIONS
1. Hemorrhage
 Blood vessels damaged as ulcer erodes into the
muscles of stomach or duodenal wall
 Coffee ground vomits or occult blood in tarry stools
2. Perforation
 An ulcer can erode through the entire wall.
 Bacteria and partially digested food spill into
peritoneum, resulting in acute peritonitis.
3. Narrowing & Obstruction
 Swelling and scarring can cause obstruction of food
leaving stomach, resulting repeated vomiting.

20. DIAGNOSIS
1. Endoscopy
2. X-ray studies- performed after drinking a thick
barium solutions.
3. Other test-
 Blood test for haemoglobin- for detecting
presence of anaemia.
 Stool occult blood test- for detecting blood in
stool.
 Bacterial culturing for H.Pylori

21. TREATMENT
Ulcer can be treated by following ways-
 Lifestyle changes
 Medications
 Surgery

22. LIFESTYLE CHANGES
 Eliminate substrate that can causing ulcers
 Stop drinking and/or smoking
 Stop using NSAID’s

23. MEDICATIONS
 Proton pump inhibitors (PPIs)
 Reduce acid level and allow ulcer to heal
 These include-
 Esomeprazole
 Lansoprazole
 Omeprazole
 Pantoprazole
 Rabeprazole

24. MEDICATION (CONT.)
 Antibiotics
 Used for H.Pylori induced ulcer
 Multiple combinations of antibiotics
 Taken for 2-3 weeks along with PPIs

25. MEDICATIONS (CONT.)
 Antacids- Neutralise the gastric acidity and
reduce pepsin activity
 Cytoprotective agents- protect the tissues
lining the stomach and small intestine