Peptic ulcer disease is caused by defects in the stomach or duodenal mucosa that extend through the inner lining. Common causes include Helicobacter pylori bacteria, nonsteroidal anti-inflammatory drugs, stress, and smoking. Patients experience gnawing or burning pain that is relieved by food and worsens with fasting. Diagnosis involves imaging tests like barium X-rays or endoscopy with biopsy. Treatment includes antibiotics to kill H. pylori, proton pump inhibitors to reduce acid, and surgery for complications like bleeding or perforation. Goals of treatment are to heal ulcers and prevent future recurrence.

1. PEPTIC ULCER DISEASE

2. Definition:
Peptic ulcers are defects in the gastric or
duodenal mucosa that extend through the
muscularis mucosa.

3. Anatomy of stomach and
Duodenum

4. Anatomy of stomach and
Duodenum

5. Aetiology
• Protective vs. Hostile Factors
• Helicobacter Pylori
• Nonsteroidal Anti-Inflammatory Drugs (NSAIDS)
• Gastrinoma(Zollinger-Ellison Syndrome)
• Hypercalcemia
• Genetic Factors
• Smoking
• Stress
• Alcohol and Diet
• O blood group

6. Aetiology of PUD
Normal
Increased Attack
Hyperacidity
Weak defense
Helicobacter pylori*
Stress, drugs, smoking

7. Protective vs. Hostile Factors
• Prostaglandin secretion
(decreased by aspirin,
NSAIDs and
cigarette smoking)
• Bicarbonate secreted
by stomach, duodenum,
pancreas, biliary tree
(decreased by NSAIDs)
• Mucus secretion
• Blood flow
• Rapid mucosal cell
turnover
• Increased parietal cell mass
with increased hydrochloric
acid and pepsin
• NSAIDs
• Helicobacter pylori infection
• Bile acids
• Tea, coffee in excess
• Irritant foods, chillies
• Smoking
• Alcohol
• Stress
• Corticosteroids

8. Protective vs. Hostile Factors

9. Helicobacter Pylori
• H. pylori is the etiologic factor in most patients with peptic
ulcer disease
• The method of H. pylori transmission is unclear, but seems to
be person-to-person spread via a fecal-oral route.
• • Live in deeper parts under lumen where PH is 7.4
• • Producing Urease which reduce the acidity of stomach
• • Protease – Mucous break down.

11. A duodenal ulcer caused by H.pylori A gastric ulcer caused by H.pylori

12. Symptoms
*Pain is the most common-Gnawing or Burning midepigastric pain.
Duodenal ulcer pain develops many hours after a meal when the
bulb is empty. Relieved by food and alkali & occurs in the early hours
of the morning.
In contrast, gastric ulcer pain is exacerbated with eating.
Non-specific symptoms include:
*Anorexia
*Nausea
*Fatty food intolerance
*Bloating
*Belching

13. Diagnostics
• Radiological Diagnosis (Barium Meal)
• Endoscopic Diagnosis
(Esophagogastroduodenoscopy (EGD)
with Biopsy
• Laboratory Testing (Urea breath tests,
Urease test,Serologic,
stool antigen testing )

14. Endoscopy

15. Endoscopy

16. Barium X-Ray

17. Histological examination

18. Urea breath test(UBT)
Urea labelled with non radioactive isotope 13C,or a
very small dose of radioactive 14C,is drunk by the
patient.If H.pylori is present in the stomach,its
powerful urease catalyses hydrolysis of urea,and
labelled carbon dioxide can be detected in breath
samples.

19. Urease test
The Urease Test consists of a twin well cartridge containing
urea, phenol red and buffer salts when reconstituted, and a
buffer. If the urease enzyme of Helicobacter pylori is present
in a biopsy specimen, the rise in pH associated with the
hydrolysis of urea causes a change in colour from yellow to
pink/red. The colour change indicates a positive reaction
and confirms the presence of Helicobacter pylori.

20. ELISA

21. TREATMENT
• Conservative
Therapy
• Operative
Therapy
• Endoscopic
Therapy
• Radiological
Therapy

22. TREATMENT
• The principles of medical treatment are :
(i) withdrawal of ulcerogenic drugs - aspirin,
phenylbutazone, corticosteroids, etc.;
(ii) stop smoking and alcohol, and restrict
intake of tea or coffee to two cups a day;
(iii) adequate physical and mental rest;
(iv) diet;
(v) antacids and
(vi) other drugs.

23. Medical Therapy
The goal of medical therapy for peptic ulcer disease is to relieve
symptoms, heal craters, prevent recurrences, and prevent
complications.
1.Antacids-Magnesium hydroxide neutralize gastric acid.It is to
be taken in relatively large doses 1 and 3 hours after meals
and at bedtime.
2.Histamine H2-receptor antagonists-cimetidine, ranitidine,
famotidine and nizatidine reduce gastric acid production by
blocking the H2 receptor on the parietal cell.
3.Proton Pump inhibitors, or PPIs -omeprazole, lansoprazole,
pantoprazole, rabeprazole, and esomeprazole inactivates the
parietal cell hydrogen-potassium ATPase and this reduce acid
secretion.
4. Sucralfate forms a barrier or coating over the ulcer crater,
stimulates prostaglandin synthesis, and binds to noxious
agents such as bile salts.Stimulates prostaglandins, which
promote improved mucosal integrity and enhance epithelial
regeneration.
5.Misoprostol is a protaglandin E1 analog that increases mucosal
resistance and inhibits acid secretion to a minor degree.

24. Medical Therapy
Treatment Regimens for Helicobacter pylori Eradication
• Triple Therapies Bismuth subsalicylate 525 mg QID
+ Metronidazole 250 mg QID + Tetracycline 500 mg
QID or Proton pump inhibitor BID + Amoxicillin
1000 mg BID + Clarithromycin 500 mg BID
• Quadruple Therapy Bismuth subsalicylate 525 mg
QID + Proton pump inhibitor BID + Metronidazole
250 mg QID + Tetracycline 500 mg QID
Note: Treatment for 10–14 days recommended.

25. Surgical Therapy
• Failure of the ulcer to completely heal
after an adequate trial of medical or
endoscopic therapy.
• Complications such as *
*Hemorrhage
*Perforation
*Penetration
*Gastric outlet obstruction
remain the major indications for
surgical intervention.

26. Surgical Procedures
* Vagotomy
-Truncal vagotomy with drainage
-Selective vagotomy with drainage
-Proximal gastric vagotomy without a drainage procedure
*Vagotomy with antrectomy
*Subtotal gastrectomy

27. Surgical technique of pyloroplasty
and truncal vagotomy

28. Selective Vagotomy

29. Antrectomy & truncal vagotomy for
duodenal ulcer with Billroth
I anastomosis

30. Endoscopic Therapy
1. Injection therapy,
2. Coagulation therapy,
3. Hemostatic clips,
4. Argon plasma coagulator,
5. Combination therapy.

31. • Injection therapy is performed with epinephrine in a
1:10,000 dilution or with absolute alcohol.
• Thermal endoscopic therapy is performed with a
heater probe, bipolar circumactive probe, or gold
probe. Pressure is applied to cause coagulation of
the underlying artery (coaptive coagulation).
• Combination therapy with epinephrine injection
followed by thermal coagulation appears to be more
effective than monotherapy for ulcers with a visible
vessel, active hemorrhage, or adherent clot.
• Hemoclips have been used successfully to treat an
acutely bleeding ulcer by approximating 2 folds and
clipping them together. Several clips may need to be
deployed to approximate the gastric ulcer folds. In
treating high-risk bleeding ulcers, combined therapy
with epinephrine and hemoclips seems to be more
efficacious than injection alone.

32. A, Endoscopic view of an actively bleeding
ulcer; B, cross-section of the stomach wall.

33. Thermally Active Methods
• Heating leads to edema, coagulation
of tissue proteins, and contraction of
arteries.
• Heat may be produced by tissue
absorbtion of laser light energy,
passage of electrical current through
tissue, or heat diffusion from another
source.

34. Endoscopic laser coagulation of
a bleeding ulcer.

35. Electrocoagulation
A, Endoscopic cauterization of a bleeding
ulcer using BICAP electrocoagulation; B,
corresponding endoscopic view.

36. Heater Probe

37. Injection Therapy
• A sclerotherapy catheter with a small retractable
needle is passed through the biopsy channel of
the endoscope. Non-bleeding visible vessels are
treated by the injection of a solution at three or
four surrounding sites about 1-3 mm from the
vessel. Subsequently, the visible vessel is injected.
In cases of bleeding vessels, injections are made
around the bleeding point until hemostasis is
achieved. This is followed by injection into the
vessel

38. Mechanical Therapy
• Endoscopic hemoclips have recently been
developed and made their way to the scene
of endoscopic therapy for peptic ulcer
disease.

39. Radiological Therapy
Angiography is an embolisation
technique for the treatment of peptic
ulcers

40. Complications of Peptic Ulcers
• The major complications of peptic
ulcer disease include
1. Bleeding,
2. Perforation,
3. Penetration,
4. Gastric outlet obstruction.

41. Perforation
• Approximately 5–10% of patients with peptic ulcers.
• Two types of perforation of the stomach
and duodenum have been observed.
*Free perforation occurs when duodenal or gastric
contents spill into the abdominal cavity with
peritoneal contamination by gastric, pancreatic and
biliary juices. Clinically this produces an acute
abdomen.
*Contained perforation occurs when the ulcer
produces a full-thickness hole in the duodenum or
stomach, but the omentum or other adjacent organs
prevent peritoneal contamination.

42. Penetration
5 to 10% of perforating ulcers may erode
through the entire thickness of the gastric
or duodenal wall into adjacent abdominal
organs. Such penetration can involve
the pancreas, bile ducts,liver, and the small
or large intestine. The pancreas is the most
common site of penetration

43. Gastric Outlet Obstruction
• Fewer than 5% of patients develop gastric outlet
obstruction from pyloric stenosis. Duodenal ulcers
give rise to pyloric stenosis more often
than gastric ulcers. Peptic ulcer disease may be
accompanied by varying degrees of obstruction
caused by inflammatory swelling of the pyloric
channel or chronic scarring associated with fibrosis.

44. Thank you for your attention