This document summarizes the pathology of various stomach conditions, including congenital abnormalities like pyloric stenosis, acute and chronic gastritis caused by factors like H. pylori infection, peptic ulcer disease stemming from an imbalance between protective and damaging forces in the stomach, and gastric carcinoma. Pyloric stenosis presents in infants as projectile vomiting. Chronic gastritis can lead to atrophy and intestinal metaplasia. H. pylori infection is a major driver of chronic gastritis and peptic ulcers. Peptic ulcers form from excessive acid exposure. Complications can include bleeding, perforation, and malignant transformation of ulcers.

1. Pathology of Stomach
Dr. Saifeldenn Hussein
Pathologist
IMS-MSU
PATHOLOGY DEPARTMENT

2. TOPICS
1) CONGENITAL ABNORMALITIES
2) ACUTE GASTRITIS
3) CHRONIC GASTRITIS
4) PEPTIC ULCER DISEASE
5) BENIGN TUMORS
6) GASTRIC CARCINOMA

4. CONGENITAL ABNORMALITIES
Pyloric stenosis:
Males 3:1 vs. females
May occur with Turner syndrome, trisomy 18, esophageal
atresia
Clinical features:
i) Narrowing of pyloris - hypertrophy and possibly
hyperplasia (muscularis)
ii) Projectile vomiting within first 3 week after birth-
dehydration
iii) Palpable mass
iv) Surgical splitting is curative

6. Diaphragmatic Hernia:
• Congenital opening defect on the diaphragm keep the
stomach and intestines move up into the chest cavity.

8. ACUTE GASTRITIS
• Gastritis (inflammation of gastric mucosa) usually transient
inflammation lead to bleeding and erosion of mucosa
Pathogenesis: associated factors:
a) NSAID (e.g., aspirin)
b) Alcohol
c) Heavy smoking
d) Stress (trauma, burns, surgery)
e) Trauma to CNS
Acid secretion damage to epithelium active inflammation
HCO3

9. CLINICAL FEATURES:
a) Asymptomatic
b) Nausea, vomiting
c) Epigastric pain
d) In severe cases: hemorrhage = severe hematemesis - melena

10. Pathology :
• Erosion of the superficial epithelial with petechial hemorrahge
any where in the stomach
• Patchy mucosal necrosis

11. CHRONIC GASTRITIS
Presence of chronic mucosal inflammation leading to:
a) mucosal atrophy
b) intestinal metaplasia
c) usually no erosion
Etiology:
a) Chronic infection (Helicobacter pylori)
b) Autoimmune (Pernicious anemia)
c) Alcohol, smoking
d) Post surgery (i.e., gastric)
e) Radiation

12. • Helicobacter pylori most important etiologic association with
chronic gastritis( Gram –ve rods with polar flagella) found
only on the epithelial surface and dose not invade.
• Urease +ve (produces NH 3 and CO2 from urea)
• Plays role in other diseases:
a) Peptic ulcer
b) Gastric carcinoma
c) Gastric MALT

13. • H. pylori-induced gastritis:
i) Pangastritis – (multifocal gastric atrophy) high level of IL-B
(potent pro-inflammatory cytokines) inhibit gastric acid- lower
H + production - risk of adenocarcinoma
ii) Antral-type – low level of IL-B - high H + production - risk
of peptic ulcer

14. Investigation:
i) Serologic test for Ab
ii) Fecal bacteria detection
iii) Urea breath test
iv) Gastric biopsy- histology visualization

15. PATHOLOGY :
• lymphocytes and plasma cells seen in the lamina propria
• Lymphoid hyperplasia
• H. pylori seen on the surface mucus of epith cells

16. Autoimmune gastritis:
Chronic diffuse inflammatory disease of the body and fundus
of the stomach
High risk of gastric CA.
• < 10% of gastritis cases due to Ab against parietal cell and IF
lead to:
a) mucosal atrophy loss of acid production ( achlorhydria)
b) increased serum gastrin (G- cell hyperplasia)
c) Pernicious anemia seen with other autoimmune diseases
i) Type 1 diabetes
ii) Addison disease
iii) Hashimoto thyroiditis

17. PEPTIC ULCER DISEASE
• PU is chronic lesions, solitary occur any part of the alimentary
tract due to exposed to the aggressive acid-peptic juices
Sites :
Duodenum = 1st part
Stomach usually = antrum
Gastroesophageal junction = reflux
Duodenum, stomach in Zollinger-Ellison syndrome
Etiology:
1) H.pylori infection: 100% in duodenal ulcers and 75% in
gastric ulcers

18. Other factors promoting peptic ulceration:
• Zollinger-Ellison syndrome – multiple ulcers in stomach,
duodenum due to excess gastrin
• Chronic NSAID use – suppress prostaglandin syn
• Cigarette smoking – impair mucosal blood flow
• Corticosteroids
• Alcoholic cirrhosis, COAD – duodenal ulcer
• Chronic renal failure and hyperparathyroidism =
hypercalcemia – stimulate gastrin – acid prod.

20. Pathogenesis :
• Imbalance between defense and damaging forces
• Severe inflammation - IL-1, IL-6, IL-8,TNF - IL-8
recruits neutrophils
• H. pylori produces proteases and phospholipases enzymes
i) break down protective actions of mucus
vi) HCO 3 - in duodenum
v) H + secretion in stomach
vi) damage to mucosa and epithelial cells leakage of
nutrients (sustain H. pylori)

22. Pathology: gross
Gastric ulcer:
Site: Lesser gastric curvature in the antral and prepyloric
region= a/e chronic gastritis
Great curvature = NSAID
Size: Single, round, less than 4 cm
Edges: Sharp, not heaped-up
Base of ulcer: Smooth and clean due to peptic digestion
Duodenal ulcer:
Site : anterior or posterior wall of the first part of the duodenum
Size : solitary some time paired ulcer on both wall (kissing ulcer)
Edges: sharply demarcated

24. Microscopically:
• 4 zones identifiable:
• Superficial necrotic layer
• Zone of inflammation
• Layer of granulation tissue
• Underlying fibrous scar

26. Clinical features:
Epigastric pain is main presentation.
• The classic duodenal ulcer is characterized by
epigastric pain 1 to 3 hours after a meal.
• Gastric ulcer pain relieved by food

27. Complications:
1) Hemorrhage
2) Perforation
3) Pyloric obstruction (gastric outlet obstruction) :caused by
muscular spasm, edema, muscular hypertrophy or contraction
of scar tissue,
4) Development of combined ulcers
5) Malignant transformation of benign gastric ulcer and dose not
occur in DU.

28. TREATMENT:
• Antibiotics to eliminate H. pylori
• Blocking gastric acid secretion with histamine-receptor
blockers and proton pump inhibitors.

29. Acute gastric ulceration:
• Focal acutely development of gastric mucosal defect due to:
1) NSAID
2) Physiological Stress (stress ulcer)
3) Severe burn or trauma (Curling ulcer)
4) Intracranial injury (Cushing ulcer)
• Gross: Small and multiple ulcer found any where in stomach
and duodenum .

30. THANK YOU