Gastric Pathology
On this page
Direct answer
Helicobacter pylori, a urease-producing spiral bacterium colonising the antral mucosa, underlies most peptic ulcers, chronic gastritis, a large share of gastric carcinoma and low-grade MALT lymphoma — and eradicating it heals the ulcer and can regress the lymphoma. Antrum-predominant infection tilts toward duodenal ulcer, while corpus-predominant pangastritis with atrophy tilts toward adenocarcinoma; autoimmune gastritis attacks the corpus parietal cells and ends in pernicious anaemia. Gastric carcinoma follows two Lauren patterns — intestinal, gland-forming and environmental, and diffuse, signet-ring and driven in familial cases by CDH1 mutation, presenting as linitis plastica, the leather-bottle stomach.
What you must remember
- Acute gastritis: NSAIDs, alcohol and stress-related ulcers — Curling ulcers in extensive burns, Cushing ulcers in raised intracranial pressure; histology of neutrophils above the neck of the pits.
- H. pylori: antral-predominant gastritis with duodenal ulcer (gastrin-driven acid load; the duodenum gastric metaplasia is colonised), versus corpus-predominant atrophic gastritis with cancer risk; tests — rapid urease test on biopsy, urea breath test, stool antigen; eradication is triple or quadruple therapy.
- Peptic ulcer complications in order: bleeding is the commonest; anterior duodenal ulcers perforate; posterior duodenal ulcers penetrate and erode the gastroduodenal artery — the anatomy that decides the presentation.
- Autoimmune gastritis: anti-parietal cell and anti-intrinsic factor antibodies, achlorhydria with hypergastrinaemia driving enterochromaffin-like hyperplasia, B12 malabsorption and pernicious anaemia with macrocytosis and combined degeneration risk.
- Lauren classification: intestinal type — glandular, environmental, with H. pylori, diet and atrophic metaplastic background; diffuse type — signet-ring cells infiltrating the wall, CDH1 (E-cadherin) mutation in hereditary diffuse gastric cancer, presenting as linitis plastica.
- Early gastric cancer: carcinoma confined to mucosa or submucosa regardless of lymph node status, with far better survival — the rationale for population endoscopic screening in Japan.
- Metastatic signatures: Virchow node (left supraclavicular), Krukenberg tumours (ovarian, often signet-ring), Blumer shelf (rectovesical deposit on rectal examination), Sister Mary Joseph nodule (periumbilical).
- GIST and Menetrier: gastrointestinal stromal tumour — CD117 (c-KIT)-positive spindle or epithelioid tumour responsive to imatinib; Menetrier disease — giant rugal folds with protein-losing enteropathy from profound foveolar hyperplasia.
One organism, five diseases
The most instructive way to hold gastric pathology is to follow a single infection through its natural history. H. pylori arrives (usually in childhood, usually via contaminated water in Indian conditions), colonises the antral mucus, and the acute gastritis becomes chronic. If the pattern stays antral, somatostatin-secreting D cells are suppressed, gastrin rises, acid load increases, the duodenal bulb develops gastric metaplasia that the organism then colonises, and a duodenal ulcer forms — the patient whose pain classically eases with food and wakes him at 2 a.m. If instead the infection sweeps the corpus, parietal cells are destroyed, acid falls, atrophy and intestinal metaplasia follow, and over decades the intestinal type of adenocarcinoma may emerge on that soil.
The same bacterium drives the third and fourth diseases through lymphoid tissue: chronic antigen stimulation recruits mucosa-associated lymphoid tissue that should not be there, and low-grade MALT lymphoma develops — the tumour famous for regressing in a substantial fraction of patients after H. pylori eradication alone, a natural experiment that proved infection-dependence. The fifth disease sits outside H. pylori: autoimmune gastritis attacks the corpus from the immune side, and its pernicious anaemia and ECL hyperplasia also raise neoplastic risk. Writing the tree this way — antrum to ulcer, corpus to cancer, lymphoid tissue to lymphoma — converts a list of stomach diseases into one causal narrative.
Where students slip
Students memorise that duodenal ulcer pain is relieved by food and forget the anatomical reason complications differ — anterior wall perforates into the peritoneum, posterior wall burrows into the gastroduodenal artery, so a bleeding posterior ulcer presents as haematemesis with the clinical picture of sudden arterial loss. Second, the biopsy rule is under-applied: every gastric ulcer is biopsied because malignant gastric ulcers can look deceptively benign, whereas duodenal ulcers are almost never malignant. Third, Krukenberg and Virchow are known but shuffled — the left supraclavicular node drains the thoracic duct, and the ovarian deposits are typically bilateral and signet-ring-filled.
Frequently asked questions
Which artery is eroded by a posterior duodenal ulcer?
The gastroduodenal artery, causing major haematemesis or melaena; anterior ulcers perforate instead.
What is linitis plastica?
The leather-bottle stomach of diffuse (Lauren) gastric carcinoma — signet-ring cells infiltrating and stiffening the whole wall without forming a luminal mass.
Which gastric lymphoma may regress with H. pylori eradication?
Low-grade MALT (extranodal marginal zone) lymphoma, dependent in many cases on chronic antigenic stimulation by the organism.
Which gene is mutated in hereditary diffuse gastric cancer?
CDH1, encoding E-cadherin; prophylactic gastrectomy is considered for confirmed carriers.
Which marker defines gastrointestinal stromal tumours?
CD117, the c-KIT receptor tyrosine kinase; tumours are treated surgically and, when advanced, with imatinib.
What distinguishes Curling from Cushing ulcers?
Curling ulcers complicate extensive burns; Cushing ulcers complicate intracranial disease with direct vagal stimulation of acid secretion.