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Precancerous and gastric cancer

  • MC in Japan. MC in males
  • H.pylori > inflammation > gastritis > gastric atrophy > gastric carcinoma

Aetiology

  • Diet – high salt, smoked food, preservatives containing nitrites
  • Familial – associated with e-cadherin mutation
  • Inactivation of p53, over expression of GFs, bcl-2 gene mutation
  • HNPCC (Hereditary nonpolyposis colorectal cancer)
  • Gastric polyps
  • Pernicious anaemia
  • Chronic gastritis – type A (proximal gastric ca). type B (distal gastric ca)
  • Resection of stomach – decreased H+ sec > gastric atrophy, which is a PF

Pathology

  • Gross types
    • Cauliflower type
    • Ulcerative type
    • Leather-bottle (Linitis plastica)
  • Lauren’s classification
    • Intestinal type – favourable prognosis
      • Polypoid and superficial types are intestinal varieties – MCC is H.pylori
      • Gland formation and definite cellular architecture
      • Gastric mucosa replaced with epithelial that resembles small int. mucosa
      • MC in men and elderly; hematogenous spread, p53 inactivation
    • Diffuse type – poor prognosis
      • MC in blood group A, familial type, young people and females
      • Poorly differentiated, signet type. Early gastric wall penetration and lymphatic spread
      • Linitis plastica, ulcerative growth
  • Depending on depth of invasion
    • Early gastric ca – Japanese Classification (see pic)
      • Involvement of mucosa and/or submucosa only with or without LN involvement
      • T1 + any N
    • Advanced gastric ca – Borrmann’s classification
      • Involvement of muscularis and/or serosa with or without involvement of LNs
  • WHO histological classification
    • Adenocarcinoma (from mucous secreting cells)
    • Adenosquamous carcinoma
    • Squamous cell carcinoma
    • Undifferentiated carcinoma

Spread

  • Direct spread
    • Horizontal submucosal spread along stomach wall
    • Vertical spread by invasion to adjacent structures – pancreas, colon, liver
  • Lymphatic spread
    • Occurs by permeation and embolisation through lymphatics
    • And later to LEFT SUPRACLAVICULAR LNs (Virchow’s LN – Troisier’s sign)
  • Haematogenous spread
    • MC to liver – causes multiple liver secondaries which present as multiple hard nodules with central necrosis
    • Later to lungs and bones
  • Transperitoneal spread
    • Can cause peritoneal seedings – leads to ascites
    • Can cause Krukenberg’s tumours in ovaries (may show Bloomers shelf   – seen on rectal exam)

Clinical Presentation

  • Recent onset of loss of appetite and WL, early satiety, fatigue
  • Upper abd pain and vomiting
  • Acanthosis nigercans
  • Mass abdomen – nodular, hard, impaired resonance, mobile, moves with resp
  • Dysphagia
  • Jaundice and palpable liver (incurable if triad present HSM, Mass, Ascites)
  • Ascites
  • (+) Courvoisier sign
  • (+) Troisier’s sign
  • (+) Trousseau sign – migrating thrombophlebitis
  • Anaemia, cachexia
  • Metastatic disease – liver secondaries, ascites, secondaries in ovaries, umbilicus, supraclavicular nodes, lungs and bones

Investigations

  • Hb%, haematocrit
  • Barium meal – irregular filling defect
  • Gastroscopy with biopsy (multiple edge biopsies)
  • Endosonography – detects involvement of layers of the stomach, nodal status and whether tumour is early or advanced
  • US abdominal – liver secondaries, ascites, nodes, ovaries
  • FNAC from L.supraclavicular LN
  • Laparoscopy – to stage disease
  • CT abd and thorax – to see size, extent, infiltration, LN status, operability
  • Tumour markers – CA 72-4 (evaluates relapse), CEA, CA 19-9, CA 12-5

Treatment

  • Surgery best treatment if patient is operable
  • Chemo – Epirubicin, Cisplatin, 5-FU
  • Early growth – lower radical gastrectomy with removal of gr.omentum, ls.omentum, all LNs, spleen, tail of pancreas and later Billroth II anastomosis
  • In case of growth in OG junction – upper radical gastrectomy and oesophagogastric anastomosis
  • In case of growth in body or linitis plastica – total gastrectomy with oesophagojejunal anastomisis

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