Topic 39 of 74 in the MU Sofia syllabus for Surgery (Medicine, Year 5). The free AceMed note covers it in 2 sections, about 322 words (2 min of reading), with 15 flashcards.
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TOPIC 39
Benign tumours of the stomach and precancerous conditions
Benign tumours of the stomach and precancerous conditions
BENIGN GASTRIC LESIONS
Benign gastric lesions include hyperplastic polyps, fundic gland polyps, adenomas, leiomyomas, lipomas, schwannomas and some gastrointestinal stromal tumours (GISTs) with low-risk features.
Most are asymptomatic and found incidentally during endoscopy. Larger lesions may cause bleeding, anaemia, pain, obstruction or intussusception.
Histology matters: gastric adenomas are dysplastic and carry malignant potential; GIST risk depends on size, mitotic rate, site and rupture.
PRECANCEROUS CONDITIONS
Chronic H. pylori gastritis may progress through atrophy, intestinal metaplasia, dysplasia and adenocarcinoma (Correa cascade).
Autoimmune metaplastic atrophic gastritis causes parietal-cell loss, achlorhydria, hypergastrinaemia, vitamin B12 deficiency and increased risk of gastric adenocarcinoma and type I gastric neuroendocrine tumours.
Intestinal metaplasia and dysplasia are risk markers; risk is influenced by extent, family history, smoking and geographic background.
Hereditary syndromes include hereditary diffuse gastric cancer (CDH1), familial adenomatous polyposis, Lynch syndrome and juvenile polyposis.
CLINICAL FEATURES & DIAGNOSIS
Symptoms are often absent or nonspecific: dyspepsia, epigastric discomfort, nausea, early satiety, occult bleeding or iron-deficiency anaemia.
Upper GI endoscopy with targeted biopsy establishes histology and assesses lesion size, number, morphology and background mucosa. Endoscopic ultrasound helps stage subepithelial lesions and distinguish wall layers.
Test for H. pylori and assess vitamin B12/iron when atrophic gastritis is suspected. Consider genetic assessment for strong family history or syndromic features.
Differential diagnosis includes early gastric cancer, lymphoma, GIST, ectopic pancreas and inflammatory lesions.
MANAGEMENT
Management is lesion-specific. Small fundic gland polyps without dysplasia may need no intervention unless associated with polyposis or atypical features.
Hyperplastic polyps may regress after H. pylori eradication; larger, symptomatic or dysplastic lesions are often removed endoscopically.
Gastric adenomas should generally be completely resected endoscopically when feasible, with surveillance based on histology and background mucosa.
Subepithelial lesions require risk assessment by size, appearance, growth and EUS findings; selected GISTs or concerning lesions require resection.
Eradicate H. pylori and arrange surveillance for extensive atrophy, intestinal metaplasia or dysplasia according to guidelines. Complications include bleeding, obstruction, malignant transformation and post-resection recurrence.
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