Professional Documents
Culture Documents
CAUSES
A probable factor in developing gastric cancer is a Helicobacter pylori infection leading to
atrophic gastritis (inflammation and damage to the inner layer of the stomach). Dietary factors
linked to gastric cancer are associated with either gastric irritation or exposure to mutagenic or
carcinogenic compounds. They include a high intake of smoked foods, salted fish and meat,
nitrite-preserved foods, starch, and fat, along with a low intake of fruits, vegetables, and animal
proteins. Associated environmental factors include exposure to ionizing radiation and being em-
ployed in metal products or chemical industries. Physiological factors are related to a rise in gastric
pH or the formation of mutagenic or carcinogenic compounds. Other associated conditions include
gastric ulcers, gastric polyps, pernicious anemia, intestinal metaplasia, achlorhydria, hypochlor-
hydria, gastric atrophy, and chronic peptic ulcers. Similarly, patients who have undergone a partial
gastrectomy for benign gastric disease are predisposed to developing gastric cancer.
GENETIC CONSIDERATIONS
Genetic factors that are linked to an increased incidence of gastric cancer include a family
history of stomach cancer and type A blood. There is a familial cancer syndrome with an
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autosomal dominant pattern of transmission identified as hereditary diffuse gastric cancer. Mu-
tations in the gene E-cadherin/CDH1 are associated with this disease. Family history has also
been associated with gastric cancer, with the risk of gastric cancer having a two-fold increase
when a first-degree relative is affected.
ASSESSMENT
HISTORY. Gastric cancer may not produce symptoms until the disease is very advanced. About
one-third of the patients report a long history of dyspepsia (painful digestion). The most common
initial symptoms are mild epigastric discomfort, loss of appetite, nausea, and a sense of
fullness or gas pains. Patients may also report experiencing unusual tiredness, abdominal pains,
constipation, weight loss, and a bad taste in the mouth. Massive GI bleeding is unusual, although
chronic bleeding may occur, which results in a positive occult blood test. Patients with advanced
gastric cancer report the classic symptoms of anemia, such as fatigue and activity intolerance,
as well as vomiting (coffee ground or sometimes containing frank blood), anorexia, abdominal
pain, dyspepsia, and dysphagia (difficulty swallowing).
PHYSICAL EXAMINATION. In the early stages of gastric cancer, the patient usually appears
healthy. The most common initial symptoms are mild epigastric discomfort, loss of appetite,
nausea, and a sense of fullness or gas pains. In later stages, patients may appear weak, pale,
dyspneic, and fatigued from anemia; they are thin and seem to be malnourished. Only 37% of
patients have a palpable abdominal mass. Observe for abdominal swelling and ascites (poor
prognostic sign) and palpate for hepatomegaly secondary to liver or peritoneal metastases. Some
patients may have palpable lymph nodes, especially the supraclavicular and axillary nodes.
Gastric cancer is frequently staged using the TNM classification system (T: primary tumor,
N: lymph node, M: distant metastasis).
PSYCHOSOCIAL. Survival rates after treatment for gastric cancer remain discouraging (the
5-year survival rate is 27% for all gastric cancers), and patients with gastric cancer have special
psychosocial concerns. Assess their support systems and their ability to cope with major lifestyle
changes. As appropriate, assess their transition through the various stages of death and dying.
Diagnostic Highlights
General Comments: The presence of lactic acid and a high lactate dehydrogenase
level in the gastric juice are suggestive of cancer. Often, in patients with gastric cancer,
plasma tumor markers (carcinoembryonic antigen [CEA], cancer antigent [CA] 19– 9) are
elevated. Positive fecal occult blood tests are associated with the chronic bleeding that
is related to gastric cancer.
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Other Tests: Cytology studies of the specimens obtained, computed tomography scan,
abdominal ultrasonography, and laparoscopy; complete blood count, CEA, CA 19– 9
Pharmacologic Highlights
Medication or
Drug Class Dosage Description Rationale
Chemotherapeutic Varies with drug Used as adjuvant (in addition Treat cancer that has me-
agents to) or neoadjuvant (before sur- tastasized to organs be-
gery) often in combination: flu- yond stomach; shrink tu-
orouracil, doxorubicin, methyl- mors before surgery
1-(2-Chloroethyl)-3-Cyclohexyl-
1-Nitrosourea (CCNU), cispla-
tin, methotrexate, etoposide;
Trastuzumab combined with
cisplatin and capecitabine or 5-
FU (for people who have not
have previous chemotherapy)
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Other Drugs: Antiemetics may be used to control nausea, which increases as the tumor
enlarges. In the advanced stages, the physician may prescribe sedatives, narcotics, and
tranquilizers to increase the patient’s comfort. Antispasmodics and antacids may also
help relieve GI discomfort.
Independent
PREOPERATIVE. Explain all preoperative and postoperative procedures. Preoperative needs
include nutritional adequacy, intravenous fluids, and prophylactic bowel preparation. Inform
the patient about the need for GI decompression via a tube for 1 to 3 weeks postoperatively.
Explain the amount of pain that should be anticipated and reassure the patient that analgesia
provides relief. Teach coughing and deep-breathing exercises and have the patient practice them.
POSTOPERATIVE. Maintain wound care, provide adequate fluid and nutrition, manage pain,
and control symptoms. Monitor the patient for complications such as hemorrhage, intestinal
obstruction, and infection. Teach wound care and the signs and symptoms of infection. Teach
nonpharmacologic pain management techniques. As indicated, teach the signs and symptoms
of “dumping syndrome”: epigastric fullness, nausea, vomiting, abdominal cramping, and diar-
rhea that occur within 30 minutes of eating. Teach patients that they may also experience
sweating, dizziness, pallor, and palpitations related to the dumping syndrome. To relieve the
symptoms, teach patients to avoid drinking fluids within a half hour of meals and to eat small
meals that are low carbohydrate, high fat, and high protein.
Gastritis 421
DOCUMENTATION GUIDELINES
• Physical findings related to gastric cancer: Epigastric discomfort, dyspepsia, anorexia, nausea,
sense of fullness, gas pains, unusual tiredness, abdominal pains, constipation, weight loss,
vomiting, hematemesis, blood in the stool, dysphagia, jaundice, ascites, bone pain
• GI decompression data: Irrigation and patency of tube, assessment of bowel sounds and pas-
sage of gas, complaints of nausea, amount and description of gastric fluid output
• Presence of postoperative complications: Hemorrhage, obstruction, anastomotic leaks, infec-
tion, peritonitis
• Presence of postoperative dumping syndrome and associated patient symptoms
Gastritis is any inflammatory process of the mucosal lining of the stomach. The inflammation
may be contained within one region or be patchy in many areas. Gastric structure and function
are altered in either the epithelial or the glandular components of the gastric mucosa. The
inflammation is usually limited to the mucosa, but some forms involve the deeper layers of the
gastric wall. Gastritis is classified into acute and chronic forms.
ACUTE. The most common form of acute gastritis is acute hemorrhagic gastritis, also called
acute erosive gastritis. The gastric erosions are limited to the mucosa, which have edema and
sites of bleeding. Erosions can be diffuse throughout the stomach or localized to the antrum.
Acute nonerosive gastritis is usually caused by Helicobacter pylori, which can also lead to
chronic gastritis.
CHRONIC. The three forms of chronic inflammation of the gastric mucosa are superficial
gastritis, atrophic gastritis, and gastric atrophy. Superficial gastritis, the initial stage in the de-
velopment of chronic gastritis, leads to red, edematous surface epithelium; small erosions; and
decreased mucus content. The gastric glands remain normal. With atrophic gastritis, inflam-
mation extends deeper into the gland area of the mucosa with loss of parietal and chief cells.
Atrophic gastritis further develops into the final stage of chronic gastritis— gastric atrophy. In
this stage, there is a total loss of glandular structure.
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