Anatomy and Physiology of the Stomach
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Published: Thu, 24 May 2018
The stomach is a hollow, muscular organ just below the diaphragm that stores the food during eating, secretes digestive juice, mixes food with these juices, and propels partially digested food, called chime into the duodenum of the small intestine. Its major anatomic boundaries are the lower esophageal sphincter where food passess through the cardiac orifice into the stomach, greater and lesser curvatures, and the pyloric sphincter, which relaxes as food is propelled through the pylorus into the duodenum. Functional areas are the fundus, body and antrum.
Gastric motility increases with the initiations of peristaltic waves. The rate of peristaltic contractions is influenced by neural an hormonal activity
Due to eating stimulation, the stomach secretes large volumes of gastric juices including mucus, acid, enzymes,hormones, intrinsic factor and gastroferrin. (Sue & Kathryn, 2008)
Terminology of the Stomach Cancer
Cancer of the stomach is also known as stomach carcinoma or gastric carcinoma/cancer.
Adenocarcinoma is the most significant malignant tumor of the stomach and accounts for 97% of all malignant lesions in the stomach. This name implies that the cancer is located in the stomach (gastric), affects cells that would normally make up glands (adeno-) and has malignant potential (-carcinoma). Other forms of stomach cancer include lymphomas, which involve the lymphatic system and sarcomas, which involve the connective tissue (such as muscle, fat, or blood vessels).
Morphologically, gastric carcinoma is classified into four distinct types: (1) the fungating or polypoid type, which has the best prognosis; (2) the ulcerating type, which arises as growth away from the lumen and may be confused with a benign ulcer; it appears in the early life of the cancer and is the most common type of cancer, accounting for 30% of all the stomach cancers; (3) the superficial spreading type; and (4) a diffuse spreading type referred to as linitis plastic/ scirrhous carcinoma, which accounts for 10% of all gastric carcinomas. It is common for the diffuse type to infiltrate the walls before the layers bulge into the lumen. The involved part becomes contracted, thick-walled, and firm. It begins and encircles the pylorus and causes obstruction. The prognosis is extremely poor, and cure is rare because of the early disease advancement prior to detection. Gastric carcinoma metastasizes very early to the liver and other organ and structures including the lungs and bone. Metastases grow in the liver, and emboli are discharged and spread via the portal venous system to the lungs and eventually to the bone. . (PATHO FOR JXR,89)
Histologically, gastric cancers tend to fall into one of two types (Lauren Classification) : (1) intestinal, malignant cells arranged in acini invade through the muscle of the stomach wall ; (2) diffuse, typically seen in linitis plastic. These tumors consist of signet ring cells. Extracellular mucin may also be present. Globules of mucin push the nucleus to one side . (robin & Fiona)
Gastric carcinomas are aggressive tumors with both local and distant spread. Local spread to oesophagus, mucosal and submucosal lymphatic spread to duodenum, to draining lymph nodes, to adjacent viscera including liver. Distant spread by lymphatics to supraclavicular node, to lungs but usually to late, hematogenous to liver via portal vein and transcoelomic to ovaries. (robin & Fiona)
CHAPTER TWO: LITERATURE REVIEW
Helicobacter pylori infection is believed to be the cause of most stomach cancer while various genetic factors and autoimmune atrophic gastritis, intestinal metaplasia are associated with increased level of risks. Smoked foods, salted fish and meat, and pickled vegetables appear to increase the risk of stomach cancer. Nitrates and nitrites are found in cured meats. They can be converted by certain bacteria, such as into compounds that have been found to cause stomach cancer in animals.. In more detail, H. pylori are the main risk factor in 65-80% of gastric cancers, causes mechanism in which it induces stomach cancer potentially involves virulence factor or chroni inflammation.
Tobacco smoking is a very important but preventable cause of gastric cancer. Smoking increases the risk of developing gastric cancer considerably; from 40% increased risk for current smokers to 82% increase for heavy smokers which is nearly twice the risk for non-smoking population. Alcohol and tobacco consumption are risk factors for the disease.
Gastric cancer shows a male predominance in its incidence as up to three males are affected for every female. Estrogen may protect women against the development of this cancer form.
Stomach cancer is an important cause of death among patients with malignancies in Malaysia and ranked as the seventh most common cancer in males in Peninsular Malaysia and tenth among females pdf. Adenocarcinomas formed the majority (72.3%) of stomach cancers in Malaysia. Pdf.
The Malaysian National Cancer Registry (NCR) report for the period 2003-2005 shows an incidence of stomach cancer of 2.2 for Malay, 11.3 for Chinese and 11.9 for Indian males per 100,000 population. Malay (1.3), Chinese (7.2) and Indian (7.2) women have rates lower than men. Malays in Peninsular Malaysia have five times less stomach cancer than Chinese and Indians. This racial difference is more marked than that noted in the Singapore cancer registry. Regional data from Kelantan has an even lower rate for Malays there (1.5 for males and 0.9 for females per 100,000 population). The incidence of Helicobacter pylori infection, a known risk factor for stomach cancer, is low among Malays.
Gastric cancer incidence varies markedly with geography. In Japan, Chile, Costa Rica, and Eastern Europe, the incidence is up to 20-fold higher than in North America, northern Europe, Africa and Southeast Asia. Mass endoscopic screening programs can be successful in regions where the incidence is high, such as Japan, where 35% of newly detected cases are early gastric cancer, tumors limited to the mucosa and submucosa. Unfortunately, mass screening programs are not cost effective in regions where the incidence is low. And fewer than 20% of cases are detected at an early stage in North America and northern Europe. In the United States, gastric cancer rates dropped by over 85% during the twentieth century.
2.3 Mortality & Morbidity
This very important malignant tumor has an especially high incidence in Japan, Chile and Italy. Its incidence has fallen in the United Kingdom and the U.S.A. since the 1930s.
Gastric cancer is still the second most common fatal malignancy after lung cancer in the world, with an estimated three quarters of a million new cases diagnosed annually.
Adenocarcinoma of the stomach was the common cause of cancer death in the united states in 1930 and remains a leading cause of cancer death worldwide, but now accounts for fewer than 2.5% of cancer deaths in the United States .The age specific incidence curve increased exponentially with age. The sharp rise occurred after 60 years of age. The difference between the age specific incidence curve in males and females widened with increasing age. Survival of patients with gastric cancer is dependent on the stage at which diagnosis is made.
2.4 Signs And Symptoms
Stomach cancer in early stages often produce no noticeable symptoms (asymptomatic) or symptoms which are not specific to just stomach cancer (non specific symptoms), but also to other related or unrelated disorders. The cancer has often reached an advanced stage which may also metastasized and induced poor prognosis by the time the noticeable symptoms occur. (Internet ca 1)
Table : signs and symptoms of stomach cancer
Stage 1 ( Early)
Stage 2 (Middle)
Stage 3 (Late)
Indigestion , heartburn
which produces burning sensation
Appetite loss especially for meat
Irritation or abdominal discomfort
Fatigue and weakness
Bloating of the stomach usually after meals
Upper abdominal pain
Occasional vomiting and nausea
Constipation or diarrhea
Loss of weight
Blood present in vomitus referred to as hematemesis. This hemorrhage is usually from the stomach
Melena, the passage of dark, tarry stools
Dysphagia, this feature suggests a tumor in the cardia or extension of the gastric tumor in to the esophagus
H.pylori has now been accepted as the major of chronic gastritis, it is logical to implicate this infection in the causation of gastric cancer. The prevalence of H.pylori infection frequently runs parallel with the incidence of gastric cancer in the same populations. Long-term infection leads to glandular atrophy which leads to a gradual decline in acid secretion. Hypochlorhydria allows other bacteria to proliferate in the gastric juice; these bacteria are capable of reducing nitrate ions to nitrite and can catalyse nitrosation of amines and amides present in the diet to give rise to potentially carcinogenic compounds.
H.pylori is capable of producing acetaldehyde. Acetaldehyde is a highly reactive product which damages epithelial cells and can cause DNA damage and can be minimized by anti-oxidant vitamins. Diets rich in fresh fruits and vegetables as protective against gastric cancer.
The most important factor underlying the relationship between H.pylori and gastric cancer is a promotional effect through high cell turnover. The production of cytotoxins and ammonia by the organism, and indirect epithelial damage brought about by cytokines and polymorph products, induce increased cell turnover. DNA repair is compromised by increased cell proliferation,and the probability of a mutation escaping repair and being transmitted to daughter cells is increased.
Several molecular genetic changes have been demonstrated in gastric cancer. Mutations and deletions of tumor surpressor genes have been
However while some of these mutations are consistent with exogenous chemical carcinogens or exposure to endogenous free radical injury, one cannot infer the nature of the mutational agent from the genetic lesions with any certainty. Nevertheless the overall evidence favours link between H.pylori infection and gastric cancer.
Gastric adenocarcinomas are classified according to their location in the stomach.gastric cancer with diffuse infiltrative growth pattern are more often composed of signet ring cells. Although intestinal type adenocarcinomas may penetrate the gastric wall, they typically grow along broad cohesive fronts to form either an exophytic mass or an ulcerated tumor. The neoplastic cells often contain apical mucin vacuoles, and abundant mucin may be present in the gland lumens. In contrast, diffuse gastric cancer is generally composed of discohesive cells that do not form glands but instead have large mucin vacuoles that expand the cytoplasm and push the nucleus to the periphery, creating a signet-ring cell morphology. These cells permeate the mucosa and stomach wall individually or in small clusters, which makes tumor cells easy to confuse with inflammatory cells, such as macrophages,at low magnification. Extracellular mucin release in either type of gastric cancer can result in formation of large mucin lakes that dissect tissue planes. Kumar ababss
A mass may be difficult to appreciate in diffuse gastric cancer, but these infiltrative tumors often evoke a demoplastic reaction that stiffens the gastric wall and may provide a valuable diagnostic clue. When there are large areas of infiltration diffuse rugal thickening and a rigid, thickened wall may impart a leather bottle appearance termed linitis plastic. Breast and lung cancers that metastasize to the stomach may also create a linitis plastic-like appearance Kumar ababss
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