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GASTRIC CA Ruanto, M.T., Sabalvaro, D.K., Salac, C.N., Salazar, J.

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Presentation on theme: "GASTRIC CA Ruanto, M.T., Sabalvaro, D.K., Salac, C.N., Salazar, J."— Presentation transcript:

1 GASTRIC CA Ruanto, M.T., Sabalvaro, D.K., Salac, C.N., Salazar, J.
References: Harrison’s Principle of Internal Medicine 17th edition

2 EPIDEMIOLOGY GASTRIC ADENOCARCINOMA
Decrease incidence and mortality rates for gastric CA during past 75 years (unclear reasons) Risk: lower > higher socioeconomic classes Development: Environmental exposure beginning early in life Dietary carcinogens

3 EPIDEMIOLOGY PRIMARY GASTRIC LYMPHOMA
Uncommon: <15% of gastric malignancies ~2% of all lymphomas Stomach – most frequent extranodal site for lymphoma Increased in frequency during the past 30 days Detected during the 6th decade of life

4 EPIDEMIOLOGY GASTRIC (NONLYMPHOID) SARCOMA
Leiomyosarcomas & GIST: 1-3% of gastric neoplasms

5 CLINICAL FEATURES ADENOCARCINOMA
Asymptomatic - superficial & surgically curable insidious upper abdominal discomfort (vague, postprandial fullness to severe steady pain) - extensive tumors Anorexia with slight nausea Weight loss, nausea & vomiting - tumors of the pylorus dysphagia & early satiety - diffuse lesions originating in cardia No early physical signs Palpable abdominal mass – long-standing growth, regional extension

6 CLINICAL FEATURES ADENOCARCINOMA Metastases: Malignant ascites
intraabdominal lymph nodes supraclavicular lymph nodes Ovary (Krukenberg’s tumor) Periumbilical region (“Sister Mary Joseph node”) Peritoneal cul-de-sac (Blumer’s shelf): palpable on rectal or vaginal examination Malignant ascites Liver – most common site for hematogenous spread of tumor Unusual clinical features: migratory thromboplebitis, microangiopathic hemolytic anemia & acanthosis nigrans

7 CLINICAL FEATURES PRIMARY GASTRIC LYMPHOMA
Epigastric pain, early satiety & generalized fatigue Ulcerations with ragged, thickened mucosal pattern by contrast radiographs GASTRIC (NONLYMPHOID) SARCOMA Anterior and posterior walls of gastric fundus most frequently involved Ulcerate and bleed Rarely invade adjacent viscera Do not metastasize to lymph nodes May spread to liver and lungs

8 DIAGNOSIS Double contrast radiographic examination Gastroscopy
Simplest procedure – epigastric complaints Helps detect small lesions by improving mucosal detail Stomach should be distended  decreased distensibility may be the only indication of diffused infiltrative carcimoma Gastroscopy Not mandatory if: Radiographic features are typically benign Complete healing can be visualized by x-ray within 6 weeks Follow-up contrast radiograph obtained several months later shows a normal appearance

9 DIAGNOSIS Gastroscopic biopsy and brush cytology
Should be made as deeply as possible Recommended in all patients with gastric ulcers  to exclude malignancy Malignant ulcers must be recognized before they penetrate into surrounding tissues Rate of cure of early lesions limited to mucosa and submucosa is >80%

10 Staging system for gastric ca
Stage TNM Features No. of Cases % 5 year survival, % TisN0M0 Node negative; Limited to mucosa 1 90 IA T1N0M0 Invasion of lamina propria or submucosa 7 59 IB T2N0M0 Invasion of muscularis propria 10 44 II T1N2M0 T2N1M0 Node positive; invasion beyond mucosa but within wall 17 29 T3N0M0 Node negative, extension through wall IIIA T2N2M0 T3N1-2M0 Node positive; invasion of muscularis propria or through wall 21 15 IIIB T4N0-1M0 Node negative; adherence to surrounding tissue 14 9 IV T4N2M0 Node positive; adherence to surrounding tissue 30 3 T1-4N0-2M1 Distant metastases

11 Risk factors

12 Reference: Harrison’s Principles of Internal Medicine, 17th ed.
H. Pylori infection a major cause of stomach cancer, especially cancers in the lower (distal) part of the stomach. may lead to inflammation (chronic atrophic gastritis) and pre-cancerous changes of the inner lining of the stomach Gender Stomach cancer is more common in men than in women. Aging There is a sharp increase in stomach cancer after the age of 50. Most people diagnosed with stomach cancer are in their late 60s, 70s, and 80s. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

13 Reference: Harrison’s Principles of Internal Medicine, 17th ed.
Ethnicity It is most common in Asian/Pacific Islanders. Diet An increased risk of stomach cancer is seen with diets containing large amounts of smoked foods, salted fish and meat, and pickled vegetables. Nitrates and nitrites are substances commonly found in cured meats. They can be converted by certain bacteria, such as H. pylori, into compounds that have been found to cause stomach cancer in animals. On the other hand, eating fresh fruits and vegetables that contain antioxidant vitamins (such as A and C) appears to lower the risk of stomach cancer. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

14 Reference: Harrison’s Principles of Internal Medicine, 17th ed.
Tobacco use Smoking increases stomach cancer risk, particularly for cancers of the upper portion of the stomach closest to the esophagus. The rate of stomach cancer is about doubled in smokers. Obesity Being very overweight or obese has emerged as a possible cause of cancers of the cardia (the part of the stomach nearest the esophagus), but the strength of this link is not yet clear. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

15 Previous stomach surgery
This may be because it allows more nitrite-producing bacteria to be present. Also, acid production goes down after ulcer surgery, and there may be reflux (backup) of bile from the small intestine into the stomach. The risk continues to increase for as long as 15 to 20 years after surgery. Pernicious anemia Certain cells in the stomach lining normally make intrinsic factor (IF), which is a substance needed to absorb vitamin B12 from foods. People without enough IF may end up with a vitamin B12 deficiency, which affects the body's ability to make new red blood cells. Menetrier disease a condition in which excess growth of the stomach lining leads to the formation of large folds in the lining and to low levels of stomach acid. Because this disease is very rare, the exact increase in the risk of stomach cancer is not known. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

16 Inherited cancer syndromes
Hereditary diffuse gastric cancer is an inherited condition that greatly increases the risk of developing stomach cancer. This condition is quite rare, but the lifetime stomach cancer risk among affected people is about 70% to 80%. Researchers recently discovered the gene (E-cadherin/CDH1) responsible for this condition. Hereditary non-polyposis colorectal cancer (HNPCC, also known as Lynch syndrome) and familial adenomatous polyposis (FAP) are also inherited genetic disorders. They cause a greatly increased risk of getting colorectal cancer and a slightly increased risk of getting stomach cancer in family members who have these gene mutations. People who carry mutations of the inherited breast cancer genes BRCA1 and BRCA2 may also have a higher rate of stomach cancer. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

17 Reference: Harrison’s Principles of Internal Medicine, 17th ed.
Type A blood For unknown reasons, individuals with Type A blood have an increased risk of developing gastric cancer. Family history of gastric cancer People with several first-degree relatives who have had stomach cancer are more likely to develop this disease Epstein-Barr infection Epstein-Barr virus has also been found in the stomach cancers of about 5% to 10% of people with this disease. These people tend to have a slower growing, less aggressive cancer with a lower tendency to spread. Reference: Harrison’s Principles of Internal Medicine, 17th ed.

18 TREATMENT

19 SURGICAL TREATMENT Complete surgical removal of the tumor with resection of adjacent lymph nodes Only chance for cure Possible in <1/3 of patients Subtotal gastrectomy – distal carcinomas Total or near-total gastrectomies – more proximal tumors Extended lymph node dissection – an added risk for complications, do not enhance survival

20 SURGICAL TREATMENT Prognosis depends on the degree of tumor penetration into the stomach wall. Adversely influenced by regional lymph node involvement, vascular invasion, and abnormal DNA content Probability of survival after 5 years ~20% for distal tumors <10% for proximal tumors Recurrences continuing for at least 8 years after surgery For patients whose disease is “incurable” by surgery with no ascites or extensive hepatic or peritoneal metastasis: Resection of the primary lesion should still be offered. Reduction of tumor bulk – best form of palliation; enhance probability of benefit from subsequent therapy

21 Radiation Therapy Major role: palliation of pain
Gastric adenocarcinoma is a relatively radioresistant tumor. Control of tumor requires doses of irradiation exceeding the tolerance of surrounding structures (eg., bowel mucosa and spinal cord). Survival in the setting of surgically unresectable disease limited to the epigastrium was slightly prolonged when 5- FU was given in combination with radiation therapy. 5-FU: radiosensitizer

22 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.

23 Thank You!


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