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Gastric neoplasms risks and types, Gastric Polyps, Gastric leiomyoma and Gastric Cancer

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Gastric neoplasms are abnormal growths or tumors that arise from the tissues of the stomach. They can be benign (non-cancerous) or malignant (cancerous), and they originate from different types of stomach cells, such as glandular, muscle, immune, or neuroendocrine cells.

Gastric neoplasms

Gastric neoplasms are tumors or abnormal growths that occur in the stomach. Some are benign (non-cancerous and usually harmless). Some are malignant (cancerous and dangerous). They can develop from different kinds of stomach cells, like:

  • The cells lining the stomach (leading to adenocarcinoma).
  • Muscle cells (GIST tumors).
  • Immune cells (lymphomas).
  • Hormone-producing cells (carcinoid tumors).

Blood supply

  • The left gastric artery → from the coeliac artery.
  • The right gastric artery→ from the common hepatic artery.
  • Right gastro-epiploic artery→ from the common hepatic artery.
  • Left gastro-epiploic artery→ from the splenic artery.
  • Short gastric arteries → from the splenic artery.
  • The corresponding veins drain into the portal system. The lymphatic drainage of the stomach corresponding its blood supply.

Lymphatic Drainage into 4 Zones

  • Superior gastric.
  • Suprapyloric.
  • Pancreaticolienal.
  • Inferior gastric/subpyloric.

All four drain into the celiac group of nodes and into the thoracic duct. Gastric cancers drain into any of these groups regardless of the location of the tumor.

Gastric neoplasms

Gastric neoplasms

Lymphatic Drainage

Lymph nodes draining the stomach are numbered and divided into 4 levels, as follows:

  1. Level 1: (Perigastric lymph nodes) – Right paracardiac (1), left paracardiac (2), along lesser curvature (3), along greater curvature (4), suprapyloric (5), infrapyloric (6)
  2. Level 2: Along LGA (7), along CHA (8), along celiac axis (9), at splenic hilum (10), along splenic artery (11)
  3. Level 3: In hepato-duodenal ligament (12), behind the duodenum and the pancreas head (13), at the root of the small bowel mesentery (14)
  4. Level 4: Mesocolic (15), paraaortic (16)

Stomach Innervations

  1. Parasympathetic innervation of the Stomach → Vagus nerve
  2. 90% of the fiber in the vagal trunk is afferent (info-transmitting from the stomach to the CNS).
  3. Sympathetic innervation of the Stomach – Splanchnic Nerve.
  4. Derived from spinal segments T5-T10

The stomach has 5 Layers (from inside to outside):

  1. Mucosa: Epithelium, lamina propria, and muscularis mucosae.
  2. Submucosa.
  3. Smooth muscle layer.
  4. Subserosa.
  5. Serosa

Gastric Neoplasms

Benign:

40% mucosa-based, 40% muscularis-based

  • Epithelial: Gastric polyps.
  • Mesenchymal: Leiomyomas.

Malignant:

Primary:

  • Adenocarcinoma (94%).
  • Lymphoma (4%).
  • Gastrointestinal stromal tumors “GIST” 1%.

Secondary: Invasion from adjacent tumors.

Adenocarcinomas account for approximately 95% of all malignant gastric neoplasms. The remaining 5% of tumors are lymphomas, leiomyosarcomas, or carcinoids.

1. Gastric Polyps

Gastric polyps include:

1. Hyperplastic polyps (regenerative) polyps: These are the commonest (80%) and occur in association with gastritis and peptic ulcer (inflammatory origin).

2. Adenomatous polyps (tubular and villous):

  • True gastric adenomas are rare (only 5% of gastric polyps).
  • The majority lie in the antral lesion.
  • May be sessile, villous, pedunculated, or lobulated.
  • May be single or multiple.
  • The progression of a gastric polyp into carcinoma is very rare (contrary to what occurs in the colon).

Inflammatory fibroid polyps: rare, found in the gastric antrum.

3. Myoepithelial hamartomas (Polyps of Peutz-Jeghers syndrome): Patients with Peutz-Jeghers syndrome have an increased risk of developing carcinomas of the liver, pharynx, and stomach. This syndrome is characterized by:

  1. Polyps along the GI gut.
  2. Pigmentation of the lips.

Heterotopic pancreatic tissue

  • Benign gastric polyps are found incidentally in 2–3% of upper gastrointestinal endoscopies.
  • Their incidence increases with patient age.
  • Small polyps are almost always asymptomatic.
  • Larger polyps may bleed due to erosions or ulceration.
  • Very large distal polyps may produce obstructive symptoms.

Treatment

  • Endoscopic Excision of Gastric Polyps.
  • Polyps less than 2 cm are easily snared.
  • Larger polyps or sessile polyps are best Removed Operatively to obtain a clear margin and complete removal.

2. Gastric leiomyoma

Incidence of 16% at autopsy.

Pathology:

  • Arises from smooth muscle of the GIT tract.
  • Difficult to distinguish from GIST.
  • Differentiation only on the mitotic index.
  • 75% benign.
  • Large protruding lesions with a central ulcer. Usually present with bleeding.

Treatment is local excision with a 2–3 cm margin.

Gastric lipoma

Rare submucous lesions

  • Asymptomatic.
  • On routine endoscopy.
  • Require no treatment.

3. Gastric Adenocarcinoma (Gastric Cancer)

  • Epidemiology
  • Aetiologic factors
  • Pathology.
  • Clinical features.
  • Investigations.
  • Treatment.

Epidemiology:

Gastric cancer (GC) is the fourth most common malignant disease and the third leading cause of cancer-related death worldwide.

  • Gastric carcinoma is often diagnosed at an advanced stage, and the prognosis is still unsatisfactory.
  • Since GC is mostly asymptomatic until advanced stages, the early detection using effective screening approaches is important.
  • The disease presents most commonly in the 5th and 6th decades of life.
  • GC affects males twice as often as females.
  • Elderly: More common in males (3:1).
  • Blacks: Low SE status.
  • Incidence ↓ in the USA/western Europe.
  • Leading cause of death in Asia/Eastern Europe.

Risk factors:

1. Predisposing:

  • Pernicious anemia→ (10% risk of gastric carcinoma).
  • Previous gastric resection.
  • Gastrectomy (gastric dumping syndrome) ⇒0-5 times the risk (15 or more years).
  • Chronic gastric ulcer → It carries a small risk.
  • Chronic atrophic gastritis (achlorhydria): It is the most researched risk factor in gastric carcinoma due to: The incidence of atrophic gastritis in patients with pernicious anemia is 3-6 folds↑. Several risk factors mentioned above are thought to act by causing damage to the gastric mucosa with subsequent development of atrophic gastritis. There is now increasing evidence for the progression of gastric atrophy to intestinal metaplasia, dysplasia, and carcinoma in-situ.

2. Environmental:

  • H. Pylori infection Sero (+) patients have 6-9 folds risk.
  • Male gender, black race, low socioeconomic Status (this applies to the USA population).
  • Nationality (JAPAN).
  • Occupational hazards: miners, metal workers exposed to dusts of asbestos and wood.

3. Diet: (major role)

  • High-fat diet.
  • Pickled, preserved food & Excessive salt intake (containing polycyclic hydrocarbons, nitrosamines). Hypothesis: dietary (nitrates)⇒ bacterial proliferation in an achlorhydria stomach →↑ N-nitrosamine production⇒ stomach cancer.
  • Smoking and Alcohol⇒ It lowers vitamin levels.

On the other hand, Diets that diminish the incidence of gastric cancer.

Fresh fruit and vegetables and Vitamin C.

4. Genetic:

About 10% of cases run in families, and between 1% and 3% of cases are due to genetic syndromes inherited from a person’s parents, such as hereditary diffuse gastric cancer.

  1. Blood group A (relative risk = 1.2 times).
  2. HNPCC: Hereditary non-polyposis colon cancer.
  3. Familial Adenomatous Polyposis (FAP).
  4. Family history of gastric cancer.
  5. Genetic mutations.
  6. People who carry mutations of the inherited breast cancer genes BRCA1 and BRACA2 may also have a higher rate of stomach Cancer.

Premalignant conditions

  • Adenomatous Polyps. Villous adenomatous polyp (2%) has malignant potential
  • Chronic atrophic gastritis.
  • Benign gastric ulcer.
  • Gastric remnant.
  • Menetries disease.

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