CARCINOMA STOMACH AETIOLOGY,CLASSIFICATION & CLINICAL FEATURES BY JOSE JAMES
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CARCINOMA STOMACH AETIOLOGY,CLASSIFICATION & CLINICAL FEATURES BY JOSE JAMES
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CARCINOMA STOMACH- ETIOLOGY,CLASSIFICATION & CLINICAL FEATURES.
Jose JamesFolgen
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CARCINOMA STOMACH AETIOLOGY,CLASSIFICATION & CLINICAL FEATURES BY JOSE JAMES
- 1. CARCINOMA STOMACH AETIOLOGY,CLASSIFICATION & CLINICAL FEATURES BY JOSE JAMES S3 UNIT UNDER THE GUIDANCE OF PROF. DR. T. SIVAKUMAR, M.S
- 2. Introduction ‘It is the captain of men of death’ One of the most common causes of cancer death in the world Common in Japan Common in males (2:1) Multifactorial Aetiology
- 3. Risk Factors Genetic Diet Obesity Infections Occupation Lifestyle Others
- 4. Genetic E-cadherin gene mutation-HDGC CDH1/CD324 APC GENE Hereditary Non Polyposis Colorectal Cancer Li-Fraumeni syndrome- TP53 Blood Group A
- 6. Diet High salt diet Red meat Smoked salmon fish-polycyclic hydrocarbons Food with nitrates and nitrites- nitrosamines N-nitroso compounds
- 7. Obesity
- 8. Helicobacter pylori Infection Helicobacter pylori infection—high-risk (Cag A strain) 6 fold increase in incidence. It causes intestinal type of gastric cancer
- 9. Occupation Rubber workers Coal workers Zinc, lead, talc, asbestos
- 10. Lifestyle Smoking Alcohol NSAID
- 11. Others Agammaglobulinaemia Epstein-Barr virus infection Pernicious anemia
- 13. Precursor Lesions Chronic atrophic gastritis Intestinal metaplasia Peptic ulcer disease Menetriers disease Adenomatous gastric polyps Stomach remnants
- 14. Chronic Atrophic Gastritis Most common precursor lesion Loss of glandular tissues ATROPHIC GASTRITIS AMAG EMAG
- 15. Autoimmune Multifocal Atrophic Gastritis (Type A) • Loss of acid Proton pump • CD4+T cells • Parietal cells Auto antibodies • Vitamin B12 deficiency • Pernicious anemia Intrinsic factor
- 16. Environmental Multifocal Atrophic Gastritis(EMAG) • Inhibition of gastric bicarbonate transporters Loss of mucosal barrier • Hydrolyses urea • Produces ammonia Releases urease • Stimulation of G cells to secrete gastrin • Local gastrin production Increased acid production
- 18. Intestinal metaplasia ChronicH.pyloriGastritis Increased gastrin levels Abnormal mucosal cell growth INTESTINALMETAPLASIA Oxyntic atrophy Increased goblet cells Autoimmunegastritis Achlorhydria Bacterial overgrowth Carcinogenic nitrosamines production
- 19. Chronic Benign gastric Ulcer Chronic mucosal ulceration affecting stomach Imbalance between mucosal protective and damaging factors Develops on a background of chronic gastritis Sharply punched out defect Predominant on lesser curvature near the interface of body and antrum
- 21. Menetrier’s disease Excess production of TGH alpha Diffused hyperplasia of mucus epithelium in body and fundus Protein losing enteropathy Presents as diarrhea and weight loss Hypoplasia of parietal and chief cells
- 23. Adenomatous gastric polyps Occur in the background of gastric atrophy and intestinal metaplasia Risk increases; size > 2cm Lesion of dysplastic intestinal columnar epithelium
- 25. Stomach remnants After Billroth 2 GJ/ Vagotomy + GJ Takes > 15 years Site – close to the stoma ALTERED ACID LEVEL+ENTEROGASTRIC BILE REFLUX => ATROPHIC GASTRITIS => METAPLASIA => DYSPLASIA
- 26. Correa cycle Chronic gastritis Gastric atrophy Intestinal metaplasia Dysplasia Carcinoma in situ Carcinoma
- 29. Classification WHO LAUREN CLASSIFICATION BASED ON DEPTH OF INVASION Early (Japanese) & Advanced (Bormann) SIEWERT CLASSIFICATION MORPHOVOLUMETRIC CLASSIFICATION MING CLASSIFICATION MORSON AND DAWSON CLASSIFICATION
- 30. WHO HISTOLOGICAL CLASSIFICATION Adenocarcinoma- most common 1.Papillary adenocarcinoma 2.Tubular adenocarcinoma 3.Mucinous adenocarcinoma 4.Signet cell adenocarcinoma(poor prognosis) Adenosquamous carcinoma Squamous cell carcinoma Undifferentiated carcinoma
- 31. LAUREN CLASSIFICATION INTESTINAL Most Common Gastric mucosa is replaced with epithelium that resembles small bowel mucosa APC gene mutation Haematogenous spread, microsatellite instability, APC gene mutations, p53, p16 inactivation. DIFFUSE Less Common Poorly differentiated with gastric wall penetration Linitis plastica, ulcerative growth without glandular formation is common in this type. Decreased E-cadherin with p53, p16 inactivation.
- 32. JAPANESE CLASSIFICATION(Early) Type 1 - Protruded : tumor grows outward from stomach wall Type 2a- Superficial Elevated: tumor grows slightly above mucosa Type 2b- Superficial Flat : tumor grows flat along mucosa Type 2c- Superficial Depressed: tumor grows into mucosa Type 3 - Excavated :tumor grows through mucosa and into submucosa
- 34. BORMANN’S CLASSIFIATION(ADV.) Polypoid carcinoma Ulcerated carcinoma with clear cut margin Ulcerated carcinoma without clear cut margin Diffuse carcinoma - Linitis plastica Unclassified
- 35. LINITIS PLASTICA (Leather-Bottle Stomach) Aggressive diffuse type Enormous proliferation of fibrous tissue involving submucosa of stomach. Type IV gastric carcinoma Poorly differentiated type lacking glandular formation-clusters of small uniform cells often with signet ring cells
- 37. Common Site of Occurrence Prepyloric and pyloric region (65%) (most common site) Body (25%). Fundus, OG junction.
- 38. Clinical Presentation ASYMPTOMATIC: 1. In Early Gastric cancer and cancer of the body of stomach. NON-SPECIFIC SYMPTOMS: 1. Indigestion 2. Vague epigastric discomfort 3. Constant non-radiating pain which is not related to food intake.
- 39. SPECIFIC SYMPTOMS(LATE stage): Vomiting, Dysphagia, Mass. Depends on site of tumour. METASTATIC DISEASE(ADVANCED stage): Liver secondaries Ascites Secondaries in ovary Rectovesical pouch-Blumer shelf Umbilicus-sister Mary joseph nodule Supraclavicular nodes Lung and bone secondaries
- 40. RARE PRESENTATIONS Secondaries in liver with silent primary stomach Can present as perforation.
- 41. UNUSUAL PRESENTATIONS ACANTHOSIS NIGRICANS IRISH NODES
- 42. Recent onset of loss of weight and loss of appetite Early satiety- distal gastric carcinoma Fatigue Microcytic hypochromic anaemia(iron deficiency anaemia) is common due to bleeding from tumour. Cachexia (later) CLINICAL FEATURES
- 43. Abdominal distension Abdominal pain which is 1. vague pain 2. constant 3. not related to food 4. loss of periodicity
- 44. Presentations of gastric outlet obstruction such as 1. Visible gastric peristalsis- positive 2. Ausculto percussion test – positive 3. Succussion splash- positive The gastric outlet obstruction most commonly associated with malignancy than benign.
- 45. MASS IN ABDOMEN: mass in pylorus lies above the umbilicus nodular hard with impaired resonance mobile moves with respiration all borders well made out
- 46. Dysphagia with mass in upper epigastrium When it arises from the body of stomach it may present as only mass abdomen Ball rolling movements. Hematemesis and melena due to upper GI bleed.
- 48. Non Metastatic Effects Migrating thrombophlebitis (Trousseau sign) Deep vein thrombosis It is mainly from the effect of the tumor on thrombotic and hemostatic mechanisms.
- 49. TROUSSEAU SIGN
- 50. MODES OF SPREAD(Metastases) Direct spread Lymphatic spread Blood spread Transperitoneal spread
- 53. NODAL METASTASIS Secondaries in umbilicus as sister Mary joseph nodules which spread through ligamentum teres Presents as subcutaneous nodules around the umbilicus.
- 54. Sister Mary Joseph Nodule
- 55. Virchow's Nodes-Troisier's Sign
- 56. BLOOD SPREAD In liver causes multiple liver secondaries present as multiple hard nodules with umblications due to central necrosis Later lungs and bones can be involved
- 58. TRANSPERITONEAL SPREAD Peritoneal seedlings-Ascites Rectal secondaries [blumer shelf] Krukenberg’s tumour involving ovaries
- 62. Reference Sabiston Textbook of Surgery 20th Edition The Biological Basis of Modern Surgical Practice Schwartz's Principles of Surgery 10e Bailey & Love's Short Practice of Surgery,26th Edition SRB's Manual of Surgery 3rd Edition
- 63. THANK YOU
Hinweis der Redaktion
- Malignant tumors-93% Carcinoma-88% Lymphoma-3% Leiomyosarcoma 1.7%
- Diet and environmental
- Cadherins (named for "calcium-dependent adhesion") are a type of cell adhesion molecule (CAM) that is important in the formation of adherens junctions to bind cells with each other. Familial—10%. Napoleon. Familial gastric cancer in associated with mutation of e-cadherin gene (90% risk).hereditary diffuse gastric cancer. prophylactic total gastrectomy should be considered for patients with this mutation Impairment/lack of adhesion molecule E-cadherin ▪ Genetic mutation (germline, somatic, epigenetic methylation) of CDH1 gene → inactivation of CDH1 → non-functional E-cadherin → unregulated division (impaired tumour suppressor function); increased ability to spread, invade adjacent structures Loss of E-cadherin function or expression has been implicated in cancer progression and metastasis.[10][11] E-cadherin downregulation decreases the strength of cellular adhesion within a tissue, resulting in an increase in cellular motility. This in turn may allow cancer cells to cross the basement membrane and invade surrounding tissues APC GENE Adenomatous polyposis coli (APC) also known as deleted in polyposis 2.5 (DP2.5) is a protein that in humans is encoded by the APC gene.[4] The APC protein is a negative regulator that controls beta-catenin concentrations and interacts with E-cadherin, which are involved in cell adhesion. Mutations in the APC gene may result in colorectal cancer. Hereditary Non Polyposis Colorectal Cancer Autosomal dominant disorder Defect in mismatch gene repair These errors activate proto oncogenes and inactivate tumour suppressor genes Microsatellite instability also causes similar defects Li-Fraumeni syndrome Associated with germline mutation in TP53 gene Sarcomas, leukemia, brain tumors, breast and adrenal cortical carcinomas are commonly associated Gastric mucosa of people with blood group ‘A’ is more susceptible for carcinogens—diffuse type. It is due to different mucopolysaccharide secretion in stomach of blood group A patients who are more susceptible for carcinogens
- Schwartz's Principles of Surgery 10e -fragile histidine triad protein (FHIT) is an encoded by the FHIT gene.(DCC-methylation in deleted in colorectal carcinoma The most common genetic abnormalities in sporadic gastric cancer affect the p53 and COX-2 genes. Over two thirds of gastric cancers have deletion or suppression of the important tumor-suppressor gene p53. Additionally, approximately the same proportion have overexpression of COX-2. In the colon, tumors with upregulation of this gene have suppressed apoptosis, more angiogenesis, and higher metastatic potential. Gastric tumors that overexpress COX-2 are more aggressive tumors. Recently, a germline mutation in the CDH1 gene encoding E-cadherin was shown to be associated with hereditary diffuse gastric cancer. Prophylactic total gastrectomy should be considered in patients with these mutations. The c-met proto-oncogene is the receptor for the hepatocyte growth factor and is frequently overexpressed in gastric cancer, as are the k-sam and c-erbB2 oncogenes. Inactivation of the tumor suppressor genes p53 and p16 has been reported in diffuse and intestinal-type cancers, whereas adenomatous polyposis coli gene mutations tend to be more frequent in intestinal-type gastric cancers.
- Ingested nitrates and nitrites from preserved food are converted to nitrosamines by GI bacteria ,Fruits and vegetables rich in vitamin ‘C’ protect from carcinoma stomach The mechanism is thought to be the conversion of nitrates in the food to N-nitroso compounds by bacteria in the stomach. N-nitroso compounds are also found in tobacco smoke, another known risk factor for gastric cancer. There is likely synergism between diet and H. pylori infection, with the bacteria increasing carcinogen production and inhibiting its removal. H. pylori has been shown to promote the growth of the bacteria that generate the carcinogenic N-nitroso compounds. At the same time, H. pylori can inhibit the secretion of ascorbic acid, preventing effective scavenging of oxygen free radicals and N-nitroso compounds.
- Proinflammatory cytokines and adipokines are produced by intra-abdominal visceral fat In western countries, carcinoma stomach is more common in proximal, near OG junction. Obesity, young individual, white people, smoking, alcohol intake, gastro-oesophageal reflux, higher social status, high calorie diet and probably genetic factors are the causes for proximal gastric cancers. It is more aggressive, spreads early due to thin muscularis mucosa. It is often diagnosed late. Signet ring type is common. It carries poor prognosis. It needs esophageal resection.
- cytoxan-associated gene A (cagA) Spiral-shaped or curved bacilli, Present in almost all patients with stomach ulcers, Spreads by faeco-oral route Virulence due to Flagella , Urease, Adhesins, Toxins Host factors – increased pro-inflammatory; decreased anti-inflammatory The primary mechanism is presence of chronic inflammation. Long-term infection with the bacteria leads to gastritis, primarily within the gastric body, with ventral gastric atrophy. These include overexpression of cyclooxygenase-2 and cyclin D2, p53 mutations, microsatellite instability, decreased p27 expression, and alterations in transcription factors such as CDX1 and CDX2
- Agammaglobulinaemia X linked disease Absence of mature B cells => lack of immunoglobulins No defense against infections Prone to H.pylori infection Epstein-Barr virus infection Associated with 10% of carcinoma stomach After primary infection establishes a latent infection Causes recombinant epithelial cell DNA Pernicious anemia High risk 6 times Associated with autoimmune atrophic gastritis
- Sabiston Textbook of Surgery
- Chronic atrophic gastritis (Fig. 26-53) is by far the most common precursor for gastric cancer, particularly the intestinal subtype (see Fig. 26-52). The prevalence of atrophic gastritis is higher in older age groups, but it is also common in younger people in areas with a high incidence of gastric cancer. In many patients, it is likely that H. pylori is involved in the pathogenesis of atrophic gastritis.
- CD4+T cells Diffuse gastric atrophy Hypergastrinaemia Endocrine cell hyperplasia => metaplasia A for autoimmune-abs(parietal cells)-Atrophic gastritis-Achlorhydria-anemia(pernicious) Affects-Body and Fundus
- Associated with H.pylori Patchy mucosal atrophy Normal gastrin levels Intestinal Metaplasia => Adenocarcinoma Antral predominant-Antral ca Pan gastritis-anywhere.
- Schwartz's Principles of Surgery 10e
- Intestinal metaplasia: Risk of carcinoma depends on extent of metaplasia in mucosa. H. pylori eradication is important here. Based on histological and biochemical nature, two types are found: Complete: Glands are completely lined with goblet cells and intestinal absorptive cells indistinguishable histologically and biochemically from their small bowel counterparts. Incomplete: It contains columnar cells, goblet cells but without intestinal absorptive cells. It also can be: Type I—Mature; goblet cells secret sialomucin. Type II—Cells in different levels of dedifferentiation. Cells secrete sialomucin and an abnormal sialomucin (sulphomucin)—a small quantity. Type III—Marked dedifferentiation of cells, secreting mainly sulphomucin.
- Causes: H.pylori, NSAIDS, smoking Currently associated more with NSAIDS than H.pylori Chronic benign gastric ulcer Chronic benign gastric ulcer Carcinoma arising from benign gastric ulcer is called as ulcer cancer of stomach
- Carcinoma arising from benign gastric ulcer is called as ulcer cancer of stomach
- Ménétrier’s disease is generally considered to carry a 5% to 10% risk of adenocarcinoma.
- Chronic benign gastric ulcer Carcinoma arising from benign gastric ulcer is called as ulcer cancer of stomach
- High grade or low grade Grading – epithelial enlargement, elongation, crowding, and hyperchromasia of nuclei. (FAP) have a high prevalence of gastric adenomatous polyps (about 50%), 10 times more likely to develop adenocarcinoma of the stomach than the general population Gastric polyps greater than 1cm should be removed to confirm the diagnosis and to eliminate any risk of malignant degeneration.
- (FAP) have a high prevalence of gastric adenomatous polyps (about 50%), 10 times more likely to develop adenocarcinoma of the stomach than the general population Gastric polyps greater than 1cm should be removed to confirm the diagnosis and to eliminate any risk of malignant degeneration.
- After Billroth 2 GJ/ Vagotomy + GJ STUMP CA
- Correa described three distinct patterns of chronic atrophic gastritis: autoimmune (involves the acid-secreting proximal stomach), hypersecretory (involving the distal stomach), and environmental (involving multiple random areas at the junction of the oxyntic and antral mucosa)
- Schwartz's Principles of Surgery 10e
- SIEWERT CLASSIFICATION Proximal gastric adenocarcinoma Type1:carcinoma in Barrett's oesophagus extending to GE junction Type2: Tumour within 2cm of squamocolumnar junction Type 3 : Tumour in sub cardial region MORPHOVOLUMETRIC CLASSIFICATION -Based on ratio of invasion into muscle to mucosa in advanced carcinoma Funnel type: mucosa involvement is more compared to muscle with ratio <0.15 columnar type: equal involvement of ratio 0.75-1.25 Mountain type: muscle invasion is more with ratio <1.25 MING CLASSIFICATION Expanding -better prognosis Infiltrate -poor prognosis MORSON AND DAWSON CLASSIFICATION Nodular ulcerated fungating Linitis plastica
- 1.Papillary-Most common- Frequently associated with liver metastasis and high rate of lymph node involvement- Histology epithelial projections scaffolded by central fibrovascular core 2.Tubular adenocarcinoma characterized by irregular shaped and fused neoplastic glands with intraluminal mucus and debris 3.Mucinous-clusters and scattered tumour cells floating in abundant extra cellular mucin Signet ring adenocarcinoma signet cells characterized by large cytoplasmic mucin vacuoles and peripherally displaced crescent shaped nuclei
- Types A-Intestinal(53%)-good prognosis B-Diffuse(33%)-poor prognosis C-Others-Unclassified(14%)
- CLASSIFICATION BASED ON DEPTH OF INVASION Early gastric cancer-only mucosa and sub mucosa involved Advanced gastric cancer-involvement of muscularis or serosa Early Gastric CA 10% have nodal metastasis nodal spread depends on tumour size[>2cm]. 70% are well differentiated Cure rate with adequate gastric resection and lymphadenectomy is 95%
- POLYPOID Tumour grows outwards from the stomach wall No area of erosion or ulceration seen ULCERATED WITH CLEAR CUT MARGIN Ulcers with well defined and sharp margins not infiltrative ULCERATED WITHOUT CLEAR CUT MARGIN ulcers with irregular,hard,stiff margins deep with raised and everted edge loss of rugosity seen areas of dead tissues [necrosis] within ulcer Infiltrative Diffuse carcinoma - Linitis plastica-Involving sub mucosa and deeper layers poorly differentiated type lacking glandular formation thickening of gastric wall and loss of rugal folds type IV gastric cancer and has poor prognosis spread: transmural, intraperitoneal and lymphatic
- Diffuse carcinoma - Linitis plastica-Involving sub mucosa and deeper layers poorly differentiated type lacking glandular formation thickening of gastric wall and loss of rugal folds type IV gastric cancer and has poor prognosis spread: transmural, intraperitoneal and lymphatic
- Acanthosis nigricans is a skin condition characterized by areas of dark, velvety discoloration in body folds and creases. The affected skin can become thickened. Most often, acanthosis nigricans affects your armpits, groin and neck. An Irish node is an enlarged axillary lymph node, often associated with advanced gastric cancer
- Asymptomatic initially ▪ Early symptoms ▫ Vague constitutional symptoms (e.g. malaise, loss of appetite, dyspepsia)
- ▪ With disease progression ▫ Epigastric pain, nausea, vomiting dysphagia, weight loss
- succussion splash- positive(checked with 4-6 hrs. empty stomach).
- ▪ If GI bleeding ▫ Anaemia, melena, coffee-ground hematemesis ▪ Pseudo achalasia syndrome (difficulty moving food, liquids from oesophagus to stomach) ▫ If tumour extends to Auerbach’s plexus/obstruction occurs near gastroesophageal junction
- The Trousseau sign of malignancy or Trousseau's syndrome is a medical sign involving episodes of vessel inflammation due to blood clot (thrombophlebitis) which are recurrent or appearing in different locations over time (thrombophlebitis migrans or migratory thrombophlebitis). The location of the clot is tender and the clot can be felt as a nodule under the skin.[1] Trousseau's syndrome is a rare variant of venous thromboembolism (VTE) that is characterized by recurrent, migratory thrombosis in superficial veins and in uncommon sites, such as the chest wall and arms. This syndrome is particularly associated with pancreatic, gastric and lung cancer and Trousseau's syndrome can be an early sign of cancer[2][3] sometimes appearing months to years before the tumor would be otherwise detected.[4] Heparin therapy is recommended to prevent future clots.
- DIRECT SPREAD Horizontal submucosal spread along stomach wall Vertical spread by invasion to adjacent structures The stomach cancer tumour spreads by direct invasion into surrounding tissues and blood vessels.
- LYMPHATIC SPREAD LYMPH NODE GROUPS Perigastric nodes Along the root of major vessels Along the root of superior mesenteric artery and hepatoduodenal ligament Distant lymph nodes
- Involvement of left supra clavicular node[virchow’s node] Sign of advanced stage of metastasis of the tumor
- cannonball lung Mets
- Peritoneal seedlings-Ascites Liver Mets
- Krukenberg’s tumour involving ovaries
- Krukenberg’s tumour involving ovaries