Stomach Anatomy and Congenital Abnormalities

Stomach Anatomy and Physiology

• The stomach is a muscular organ responsible for digesting food and producing gastric juices.
• It has a mucosal lining that protects it from the acidic environment.
• This protection involves a mucus barrier, bicarbonate secretion, epithelial cell regeneration, mucosal blood flow, and prostaglandin secretion.

Congenital and Developmental Abnormalities of the Stomach

• Congenital abnormalities of the stomach are rare, but they can include:
  • Absence of the stomach
  • Dextroposition (stomach on the right side)
  • Microgastria (small stomach)
  • Cysts, duplication, and diverticula
  • Atresia (complete blockage)
  • Congenital pyloric stenosis

Congenital Pyloric Stenosis

• It occurs in 3-4 times more males than females, particularly in firstborn children.
• There is a genetic component, and siblings are 5 times more likely to be affected.
• It is associated with Turner syndrome and trisomy 18.
• It presents in the first 2-3 weeks of life with persistent projectile non-bilious vomiting.
• Characterized by hypertrophy of the circular muscle of the pyloric sphincter.

Gastritis

• Inflammation of the stomach lining associated with mucosal injury.
• Commonly caused by infectious agents, such as Helicobacter pylori, and autoimmune or hypersensitivity reactions.
• Epithelial cell damage and regeneration without inflammation is called gastropathy.
• Classification:
  • Acute - Short-term, neutrophilic infiltrate.
  • Chronic - Longer duration, mononuclear cell infiltrate (lymphocytes and macrophages).

Acute Gastritis

• Usually transient and characterized by neutrophilic infiltration, edema, vascular congestion, and potential erosion or hemorrhage.
• Causes: Heavy NSAID use, excessive alcohol consumption, heavy smoking, severe stress, systemic infection, and ischemia.
• It can be asymptomatic or present with epigastric pain, nausea, vomiting, and hemorrhage.
• A major cause of massive hematemesis, particularly in alcoholics.

Chronic Gastritis

• Characterized by longer-duration inflammation, leading to mucosal atrophy, metaplasia, dysplasia, and increased risk of gastric cancer.
• Classification:
  • Type A (Autoimmune) - Associated with pernicious anemia and autoantibodies against intrinsic factor and parietal cells. Diffuse mucosal damage of the body and fundic mucosa.
  • Type B (Antral) - Most common form, linked to Helicobacter pylori infection.

Helicobacter pylori

• Motile, gram-negative bacteria found in the antral mucosa.
• Produces urease, toxins, and adhesins to bind to the epithelium.
• Can cause:
  • Diffuse involvement of the body and antrum (pangastritis) associated with reduced acid output.
  • Infection confined to the antrum (antral gastritis) associated with increased acid output.

H. pylori Infection and Chronic Gastritis

• H. pylori affects the antral mucosa.
• Histopathology: Lymphocytic and plasma cell infiltrate, atrophy, metaplasia, and dysplasia.
• Dysplasia is a precursor lesion to gastric cancer.
• Other causes of chronic gastritis: Psychological stress, caffeine, alcohol, tobacco, radiation, bile reflux, Crohn's disease, and graft-versus-host disease.

Peptic Ulcers

• Occur in areas exposed to acid and pepsin.
• Chronic lesions, usually single, <4 cm in diameter.
• Common sites:
  • Duodenum (first part)
  • Stomach (antrum)
  • Barrett's mucosa
  • Gastrojejunostomy
  • Jejunum
  • Meckel's diverticulum

Epidemiology of Peptic Ulcers

• Remitting and relapsing nature.
• High morbidity due to pain, loss of work hours, and cost of treatment.
• More common in younger individuals (22-55 years old) for duodenal ulcers.
• More common in older individuals (40-70 years old) for gastric ulcers, with equal prevalence in men and women.

Aetio-Pathogenesis of Peptic Ulcers

• Imbalance between acid-pepsin activity and mucosal integrity.
• Factors:
  • Increased acid-pepsin activity (duodenal ulcers)
  • Impaired mucosal defense (gastric ulcers)
  • Helicobacter pylori infection (duodenitis/gastritis)
  • Other influences (smoking, alcohol, NSAIDs)

Morphology of Peptic Ulcers

• Gross appearance:
  • Duodenal ulcers: Usually located in the first part, anterior wall, and can be "kissing ulcers."
  • Gastric ulcers: Typically on the lesser curvature, body, or antrum.
• Size: <2 cm in diameter, round to oval, punched out, straight walls, variable depth.
• Base of the ulcer: Smooth, clean, adherence to liver or pancreas, scarring and puckering.

Microscopic Features of Peptic Ulcers

• Active ulcers have four zones:
  • Necrosis and fibrin
  • Nonspecific inflammation
  • Granulation tissue
  • Fibrous/scar tissue
• Adjacent mucosa often shows gastritis, with or without H. pylori.

Investigations for Peptic Ulcers

• Barium meal, blood counts, H. pylori testing, gastric function tests, endoscopy

Complications of Peptic Ulcers

• Perforation
• Bleeding
• Stenosis (pyloric, tea-pot deformity, hour-glass stomach)
• Penetration
• Carcinoma
• Intractable pain

Gastric Carcinoma

• Most common type of malignant tumor in the stomach: adenocarcinoma.
• Incidence peaks in the 5th-7th decades.
• More common in men (2:1 ratio).
• Lower socioeconomic groups and Asian/South American countries have a higher incidence.

Etiology of Gastric Carcinoma

• Genetic: Familial predisposition, blood group A, mutations in CDH1 gene.
• Environmental factors: Dietary factors (smoked meats, pickled foods, etc.)
• Premalignant conditions: Chronic gastritis, peptic ulcers, polyps.

Morphology of Gastric Carcinoma

• Sites:
  • Cardia: 10-15% (junction of esophagus and stomach)
  • Body: 25%
  • Antrum: 40-50%
  • Diffuse: 10-15%
• Gross features:
  • Exophytic (protuberant mass) or ulcerative (erosive lesion).
  • Size varies widely, 2 cm to >30 cm.

Stages of Gastric Carcinoma

• Based on depth of invasion and lymph node involvement.
• Early stage: Confined to mucosa or submucosa.
• Advanced stage: Invasion into muscularis propria or serosa, spread to lymph nodes.
• Distant metastasis: Liver, lungs, peritoneum.