1) Peptic ulcers are chronic lesions that occur in the stomach or first part of the duodenum due to an imbalance between damaging gastric acids and the mucosal defenses. 2) Common causes of peptic ulcers include infection with Helicobacter pylori bacteria, long-term use of NSAIDs, and excess stomach acid secretion. 3) Symptoms vary but often include epigastric pain that occurs one to three hours after eating and is relieved by food or antacids. Complications can include bleeding, perforation, or obstruction.

1. Peptic
ulcer
Identification
Causes
Pathogenesis
Clinical features
Complications

2. • Acute gastritis: transient mucosal
inflammation
• maybe asymptomatic or cause variable
degrees of epigastric pain, nausea and
vomiting.
• In severe cases there may be mucosal erosion ,
ulceration ,hemorrhage , hematemesis
,melena.
• Chronic gastritis: (Helicobacter pylori,
autoimmune, chronic bile reflux)
• Nausea and upper abdominal discomfort
• Symptoms are less severe but more persistent

3. Stomach, acute gastric ulcers
Ulcers

4. Erosions: breach in mucosal epithelium only
Ulcers: Breach in mucosa that penetrate through muscularis
mucosae into submucosa, muscularis propria or deeper
Peptic ulcers: chronic most often solitary, recurrent lesions can
occur in any part of GIT exposed to aggressive action of acid peptic
juices
98% - first part of duodenum or stomach in ratio of 4:1

5. PEPTIC ULCER
• impair the quality of life rather than
shorten it.
• Most common in gastric antrum and
first portion of duodenum
• Acute peptic ulceration: focal lesions as
result of NSAIDs and physiologic stress.
1cm
– Stress ulcers (shock, sepsis, trauma)
– Curling ulcers (severe burns, trauma)
– Cushing ulcers (intracranial disease)
• Peptic ulcer disease

7. Causes
• H.pylori, NSAIDs
• GERD (gastroesophageal reflux disease)
• Ectopic mucosa secreting acid
• Gastric heteropia in Meckel diverticulum

8. Pathogenesis
• Imbalance between the mucosal defense forces
& the damaging forces
• Key conditions for development of peptic ulcer
– mucosal exposure to gastric acid & pepsin and
hyperacidity, parietal cell hyperplasia, excessive
secretary response, impaired inhibition of
stimulatory mechanisms like gastrin
– Zollinger Ellison syndrome
– H. Pylori infection. 70% of PUD associated with H.
Pylori out of these 5-10% develop ulcers

9. Pathogenesis
• Imbalance between the mucosal defense forces
& the damaging forces
• Key conditions for development of peptic ulcer
– mucosal exposure to gastric acid & pepsin and
hyperacidity, parietal cell hyperplasia, excessive
secretary response, impaired inhibition of
stimulatory mechanisms like gastrin
– Zollinger Ellison syndrome
– H. Pylori infection. 70% of PUD associated with H.
Pylori out of these 5-10% develop ulcers

13. Pathogenesis:
• Co factors
• Chronic NSAID use
• Cigarette smoking
• Corticosteroid high doses
• Psychologic stress

14. Predisposing factors
• Diagnosed in middle to older age
group, may become evident in young
• Male female ratio 10:4
• Alcoholic cirhosis
• Chronic obstructive pulmonary
disease
• Chronic renal failure
• Hyperparathyroidism
• Hypercalcemia stimulate gastrin
secrtion

15. Host defenses
•Secretion of Mucus
•Secretion of bicarbonate in the surface
mucus
•Secretion of acid and pepsin containing
fluid from the gastric pits as jets
•Rapid gastric epithelial regeneration
• Robust mucosal blood flow
•Mucosal elaboration of prostaglindins
which help to maintain mucosal blood
flow

16. Pathogenesis - HelicobacterPylori
• Gram negative rod. Lies in superficial mucous layer &
among the microvilli of epithelial cells
• Present in 70% patients. Antibiotic t/m promotes
healing
• No invasion.
• Induces inflammation and immune response –
↑production of pro-inflammatory cytokines, IL-1, IL-
6, TNF,IL-8 by mucosal cells activate neutrophils
• activation of T & B lymphocytes - cause damage to
mucosa
• proliferation of lymphoid tissue(MALT),transforms
into lymphoma.

17. Morphology
• Favored sites - first portion of the
duodenum & near interface of body
and antrum of stomach
• Solitary in 80% patients, less than
0.3cm diameter, shallow, but more than
0.6cm are deep. round sharply
punched out appearance.
• Margins of crater perpendicular. mild
edema of adjacent mucosa. no
significant elevation or beading of

18. Four zones can be
seen:
1) Necrotic
fibrinoid debris
2) Active
inflammation
3) Granulation
tissue
4) Fibrous

19. Clinical picture
• Middle age to older adults,
precipitating conditions
• Epigastric pain gnawing, burning or
aching discomfort
• Duodenal ulcer: pain occurs 1-3 hrs
after a meal & typically awakens
patient in middle of night. Relieved
by alkali or food
• Gastric ulcer: The relationship
between pain & food is more
variable

20. Complications
• Bleeding
– Most frequent complication
– Accounts for 25% of ulcer deaths
• Perforation
– Occurs in only 5% of patients
– Accounts for 66% of ulcer deaths
• Obstruction from edema or scarring
• Intractable pain

21. Treatment
• Antibiotics
• Proton pump inhibitors
• H-2 receptor inhibitors
• Antacids - Neutralization of acids
• Surgery

22. TRIPLE THERAPY
• Triple therapy consists of two antibiotics and one
proton pump inhibitor for 7 to 14 days.
• Clarithromycin – 500mg tablet BD
• Amoxicillin- 1000mg BD or
• Metronidazole
• Rabeprazole or Esomeprazole 40mg per day

23. NSAIDs
Inhibit prostaglandin synthesis
Increase secretion of HCL
Reduce bicarbonate and mucus
production
Reduce glutathione synthesis
Some impair angiogensis

34. Stomach, Helicobacter pylori gastritis inflammatory infiltrate

35. Stomach, Helicobacter pylori gastritis
The presence of neutrophils within the gastric glands
signifies active inflammation

36. Stomach, chronic peptic ulcer

37. Stomach, chronic peptic ulcer

38. Stomach, Helicobacter pylori gastritis
Lamina propria

39. Stomach, Helicobacter pylori
gastritis
Neutrophils

40. Stomach, Helicobacter pylori gastritis