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Gastric cancer
The document discusses the anatomy, histology, physiology, carcinogenesis, clinical presentation, diagnosis, staging, and treatment of gastric cancer. It notes that gastric cancer typically presents with nonspecific symptoms like abdominal pain or weight loss. Diagnosis involves endoscopy with biopsy. Staging involves endoscopic ultrasound or CT scan to evaluate tumor invasion and lymph node involvement. Treatment depends on stage but may include surgery, chemotherapy, and radiation. Screening high-risk individuals can detect early gastric cancer and improve outcomes.
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Gastric cancer
- 1. Dr. kundan Junior Resident, Department of surgery Patna medical college
- 2. Anatomy The stomach J-shaped.The stomach has two surfaces (the anterior & posterior), two curvatures (the greater & lesser), two orifices (the cardia & pylorus). It has fundus, body and pyloric antrum.
- 3. a. The leftgastric artery b. Right gastric artery c. Right gastro-epiploic artery d. Left gastro-epiploic artery e. Short gastric arteries The corresponding veins drain into portal system. The lymphatic drainage of the stomach corresponding its blood supply.
- 4. Histology Consist of fourlayers serous layer muscular layer submucous layer mucous layer
- 5. PHYSIOLOGY Function: 1. Digestion offood, reduce the size of food 2. Acts as reservoir 3. Absorption of Vit. 12, iron and calcium Stimulant of Gastric secretion: 1. Gastrin -----> (+) parietal cell 2. Acetylcholine (vagus) ---> (+) gastric cells 3. Histamine (mast cells) ---> parietal & chief cells
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- 8. Spectrum of gastriccancer Proposed progression: chronic gastritis --> chronic atrophic gastritis --> intestinal metaplasia --> dysplasia --> adenocarcinoma
- 10. Risk Factors forgastric cancer Diet nitroso compounds low fruit/vegetable, high fried foods/processed meat High salt intake Obesity Smoking (HR 2-3) ? Alcohol H. Pylori Low socioeconomic status Hereditary diffuse gastric cancer 40-67% lifetime risk for men, 60-83% for women Immigrants from endemic areas maintain native country risk, risk to offspring similar to new homeland
- 15. Precursors of GastricCancer Adenomatous polyps Chronic atrophic gastritis Pernicious gastritis Menetries’s disease Previous gastric surgery for non- cancerous conditions
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- 17. Symptoms (cont’d) Dysphagia: morecommon with proximal gastric tumors Occult GI bleeding very common, overt bleeding <20%.
- 18. Signs Palpable abdominal mass:most common physical finding If cancer spreads via lymphatics… Left supraclavicular node (Virchow’s) Periumbilical node (Sister Mary Joseph) Left axillary node (Irish) Enlarged ovary (Krukenberg's tumor) Ascites
- 19. Investigations Routine blood examination lowhemoglobin , high ESR stool examination for occult blood gastric function test - will reveal gross hypo / achlorhydria Endoscopy – helpful in diagnosing early cases and taking biopsy Ultrasonography - helps in assesing thickening of agstric wall, local invasion, peritoneal involvement , ascitis CT scan - extent of the disease , lymph node involvement , liver metastasis Barium studies Staging laproscopy
- 20. Diagnosis Endoscopy Gold standard Single biopsyfrom ulcer -> sensitivity ~ 70% Seven biopsies from ulcer -> sensitivity >98% Brush cytology increases sensitivity of single biopsies, aid in multiple biopsies unclear
- 21. Preoperative Staging Abdominal /pelvic CT scanning Endoscopic ultrasound (EUS) Depth of the tumour Enlarged perigastric/coeliac lymph nodes
- 22. Endoscopic ultrasound A small,high frequency ultrasound transducer incorporated into the distal end of the endoscope. Advantages: - superior resolution. - image not compromised by intervening gases. - lesion as small as 2-3 mm in diameter can be imaged.
- 24. Barium studies False negativein as many as 50% of cases Sensitivity as low as 14% in early cases May be superior to EGD for linitis plastica EGD may be normal while “leather-bottle” will be apparent on radiograph
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- 27. Malignant Neoplasms ofthe Stomach Primary Adenocarcinoma (94%) Lymphoma (4%) Malignant GIST (1%) Haematogenous spread Breast Malignant melanoma Direct invasion Pancreas; Liver; colon; ovary
- 28. Staging of GastricCancer Two systems: Japanese classification (more elaborate and anatomic based) Western: developed by American Joint Committee on Cancer (AJCC) and International Union Against Cancer (UICC) -- more widely used Tumors at GE junction of in cardia of stomach within 5cm of GE junction Classified using esophageal staging
- 29. Gastric carcinoma CLASSIFICATION Depth ofinvasion EARLY GASTRIC CA - mucosa & submucosa ADVANCED GASTRIC CA - into or through muscularis propria Macroscopic growth pattern – Ming classification Expanding Infiltrative - "linitis plastica" Histologic subtype Intestinal Diffuse (gastric); poorly differentiated; "signet ring" cells
- 30. Gastric carcinoma CLASSIFICATION WHO Classification: 1.Adenocarcinoma: a. Papillary adenocarcinoma b. Tubular adenocarcinoma c. Mucinous adenocarcinoma d. Signet-ring cell carcinoma 2. Adenosquamous carcinoma 3. Squamous cell CA 4. Small cell CA 5. Undifferentiated CA 6. Others Lauren Classification: 1. Intestinal type (53%) 2. Diffuse type (33%) 3. Unclassified (14%) Ming Classification: 1. Expanding type (67%) 2. Infiltrative type (33%)
- 32. Histologic type: 1. Papillary 2.Tubular 3. Mucinous 4. Signet ring Mode of spread: 1. Direct 2. Lymphatic 3. Hematologic 4. Transcoelomic route
- 35. Linitis Plastica Diffuse-type gastriccancer Tumor often infiltrates the submucosa and muscularis propria Superficial biopsies may be falsely negative Combination of strip and bite biopsy needed if suspicious for linitis plastica
- 36. Linitis Plastica, “leatherbottle stomach”
- 37. Staging workup Biopsy Imaging CT: evaluatesfor metastases (M stage) 20-30% with negative CT have intraperitoneal disease at laparatomy Accuracy of 50-70% for T stage Slightly worse accuracy for N stage compared to EUS EUS: most reliable nonsurgical method to evaluate depth of invasion More accurate than CT for T stage 65-90% accurate for N stage
- 38. Staging workup PET More sensitivethan CT for detection of distant metastases. Also useful for detecting LNs Negative PET not helpful- even large tumors can be falsely negative if metabolic activity low. Most diffuse gastric cancers (signet ring) are not FDG avid
- 39. Staging workup Serologic markers CEA,CA-125, CA 19-9, CA 72-4 may be elevated but have low sensitivity/specificity None are diagnostic Preoperative elevation in markers usually pretends high risk of adverse outcome No serologic finding should exclude surgical consideration
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- 43. Treatment Locoregional (stage I-III)disease Potentially curable multidisciplinary evaluation and consideration of surgery Advanced (stage IV) disease Palliative therapy Studies indicate longer survival and better quality of life with systemic treatment
- 44. Surgery The extent ofgastric resection depends on: - tumor size - location - depth of invasion - histological type
- 45. Treatment Complete surgical resectionwith removal of LNs (only chance of cure) Possible in < 1/3 of cases Subtotal gastrectomy for distal carcinomas, total or near-total for proximal masses Reduction of tumor bulk (palliative) Chemotherapy (cisplatin + 5-FU or irinotecan) Partial response in 30-50% of patients Radiation (for pain control, no mortality benefit with XRT alone)
- 47. The Japanese ResearchSociety for Gastric Cancer The 16 lymph node locations were classified into 4 concentric groups: N1, N2, N3, N4 Periepigastric Extraepigastric
- 48. What is theideal extent of lymphadenectomy ? D0- removes less than all relevant N1 nodes D1- removes N1 nodes only - Lt and Rt cardiac - Lt and Rt gastro-epiploic - Sub and Supra pyloric D2- removes all N1 and N2 nodes - Lt gastric - Common hepatic - Celiac - Splenic hilum and along splenic artery D3- removes all N2 and N3 nodes
- 49. The residual tumor(R) classification The absence or presence of demonstrable residual tumor after conclusion of the treatment (UICC) R0 resection -no demonstrable residual tumor R1 resection- microscopically demonstrable residual tumor (e.g. diseased residual margin) R2 resection – macroscopically visible tumor Distinction between primary palliative intervention (R1&R2) vs. potentially curative ones (R0)
- 50. Prognosis Stage TNM Features %of Cases* % 5-year survival* 0 TisN0M0 Node negative; limited to mucosa 1 90 IA T1N0M0 Node negative; invasion of lamina propria or submucosa 7 59 IB T2N0M0 Node negative; invasion of muscularis propria 10 44 II T1N2M0 Node positive; invasion beyond mucosa but within wall 17 29T2N1M0 T3N0M0 Node negative; extension through wall IIIA T2N2M0 Node positive; invasion of muscularis propria or through wall 21 15 T3N1-2M0 IIIB T4N0-1M0 Node negative; adherence to surrounding tissue 14 9 IV T4N2M0 Node negative; adherence to surrounding tissue 30 3 Any M1 Distant Metastases ** Data from American Cancer Society
- 51. Pharmacologic Therapy Cisplatin+ epirubicin & infusional 5-FU or + irinotecan Complete remissions are uncommon. Partial responses in 30-50% of cases are transient. Overall influence on survival has been unclear. Adjuvant chemotherapy alone following complete resection has only minimally improved survival. Perioperative treatment and postoperative chemotherapy + radiation therapy reduce the recurrence rate and prolongs survival.
- 52. Treatment: Supportive: Nutrition (jejunalenteral feedings or total parenteral nutrition), Correction of metabolic abnormalities that arise from vomiting or diarrhea Treatment of infection from aspiration or spontaneous bacterial peritonitis. To maintain lumen patency, endoscopic laser treatment or stenting for palliation.
- 53. Screening Mostly barium studies,EGD is concerning findings Some use serum pepsinogen testing for high risk with EGD confirmation H. pylori: sensitivity 88%, specificity 41% (Japan) 5-year survival 74-80 in screened group, 46-56% for non- screened group.
Editor's Notes
- #11 HDGC: 40-67% lifetime risk for men, 60-83% for women