An 8-Month History of Vague Systemic Symptoms

Juan Carlos Munoz, MD; Nina Y. Singh, MD; Suraj A. Naik, MD

Disclosures

October 01, 2018

Gastric cancer tends to develop slowly over many years. During the early stages no specific signs or symptoms may be present. Early symptoms may include abdominal discomfort or pain, indigestion, heartburn, nausea, vomiting, early satiety, bloating, diarrhea or constipation, loss of appetite, and/or a sensation that food gets "stuck" at the level of the epigastrium. In advanced stages, patients may complain of weakness, fatigue, dysphagia, hematemesis, melena, more severe and more localized abdominal pain, unexplained weight loss, and increased abdominal girth due to ascites or tumor growth.

Before a true cancer develops, precancerous changes often occur in the mucosal lining of the stomach. Approximately 25% of patients have a history of gastric ulcer.[12] Tumor spread typically occurs via direct invasion of adjacent organs, via the lymphatic vessels, and in advanced cases through the bloodstream. Common metastatic distributions of gastric cancer include the left supraclavicular lymph node (Virchow node), the ovaries (Krukenberg tumor), the rectouterine/rectovesical cul-de-sac (Blumer shelf), or the peritoneum (manifesting as an ascitic fluid collection). A palpable umbilical nodule (Sister Mary Joseph nodule) may represent metastasis of gastric carcinoma to the pelvis or abdomen.

Early diagnosis improves the prognosis. EGD is the diagnostic method of choice; it is easy to perform, safe, and allows for sampling of tissue. Endoscopic ultrasonography can aid in determining the prognosis by evaluating the depth and extension of the tumor to adjacent structures (lymph nodes) or organs. An upper gastrointestinal series is only used when endoscopic evaluation is not available. CT scan and/or MRI can be used to assess local and potential areas of spread. Positron-emission tomography (PET) scan using 18-fluorodeoxyglucose is probably a more sensitive test than CT scan for the detection of distant metastases.[13,14] Ninety to ninety-five percent of gastric cancers are adenocarcinomas; about 4% are lymphomas, including the slow-growing, mucosal-associated lymphoid tissue (MALT) lymphoma, and about 2% are gastrointestinal stromal tumors (GISTs). Carcinoid tumors, squamous carcinoma, adenoacanthomas, and others account for the remainder of gastric cancers.

Gastric carcinomas can be classified in several ways, including by gross appearance and microscopic appearance. Upon gross appearance, gastric cancers can be ulcerative, polypoid, scirrhous (ie, diffuse linitis plastica), superficial spreading, multicentric, or Barrett ectopic adenocarcinoma. Scirrhous carcinoma, a poorly differentiated combination of mucin-producing carcinoma cells, can infiltrate the muscle wall and result in rigid, leathery scar tissue that is difficult to manipulate during endoscopic evaluation.

On the microscopic level, undifferentiated lesions or tubular, papillary, mucinous, or signet-ring cells will be seen. The Borrmann classification system categorizes gastric cancer into type I tumors, which are fungating or polypoid; type II tumors, which are ulcerating lesions with elevated borders; type III tumors, which display ulceration and invade the gastric wall; type IV tumors, which are diffusely infiltrating (ie, linitis plastica); and type V lesions, which cannot be classified. The Lauren system sorts gastric cancer histopathology as either epidemic or endemic, and it is useful in that the descriptive histopathologic entities have clinically relevant differences. Type I are expansive, epidemic-type gastric cancers of the intestine (can also be classified as Bormann types I or II) that are associated with a retained glandular structure, chronic atrophic gastritis, a clearly defined margin, and a low propensity for invasiveness. They are associated with most environmental risk factors, have a better prognosis, and are not associated with a familial history. Type II tumors, which are diffuse, poorly differentiated, and affect younger patients, are more invasive and more aggressive in females. This type has been associated with blood type A and can manifest in several members of the same family. They are also associated with mutations in the E-cadherin.[15] There are 2 staging systems: the Japanese and the more commonly used TNM classification system.[16,17]

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