1.

History and PE
(De Leon alam mo na to!)
2. Impression = UGIB secondary to gastric cancer t/c metastasis
3. Lab findings.
Laboratory Studies
The goal of obtaining laboratory studies is to assist in determining optimal therapy.
A CBC count can identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition. Approximately 30% of
patients have anemia.
Electrolyte panels and liver function tests also are essential to better characterize the patient's clinical state.
Carcinoembryonic antigen (CEA) is increased in 45-50% of cases.
Cancer antigen (CA) 19-9 is elevated in about 20% of cases.
Distinctive serum glycan patterns may have the potential to serve as markers for gastric cancer risk. In a study of 72 serum
samples from patients with gastric cancer, nonatrophic gastritis, or duodenal ulcer, Ozcan and colleagues found that abnormal
patterns of serum glycans (sugars attached to proteins) may be useful as a screening tool for identifying patients with H pylori
infection who are at risk for stomach cancer.

A total of 19 significant differences in serum glycan expression were found between
gastric cancer patients and individuals with asymptomatic nonatrophic gastritis. High-mannosetype glycans, glycans with 1
complex type antenna, and bigalactosylated biantennary glycans tended to be lower in gastric cancer patients, whereas levels of
nongalactosylated biantennary glycans were higher. Altered serum glycan levels were also seen in study patients with ulcer.
Imaging Studies
Esophagogastroduodenoscopy has a diagnostic accuracy of 95%. This relatively safe and simple procedure provides a permanent
color photographic record of the lesion. This procedure is also the primary method for obtaining a tissue diagnosis of suspected
lesions. Biopsy of any ulcerated lesion should include at least 6 specimens taken from around the lesion because of variable
malignant transformation. In selected cases, endoscopic ultrasound may be helpful in assessing depth of penetration of the tumor
or involvement of adjacent structures.
Double-contrast upper GI series and barium swallows may be helpful in delineating the extent of disease when obstructive
symptoms are present or when bulky proximal tumors prevent passage of the endoscope to examine the stomach distal to an
obstruction (more common with gastroesophageal [GE]-junction tumors). These studies are only 75% accurate and should for the
most part be used only when upper GI endoscopy is not feasible.
Chest radiograph is done to evaluate for metastatic lesions.
CT scan or MRI of the chest, abdomen, and pelvis assess the local disease process as well as evaluate potential areas of spread
(ie, enlarged lymph nodes, possible liver metastases).
Endoscopic ultrasound allows for a more precise preoperative assessment of the tumor stage. Endoscopic sonography is
becoming increasingly useful as a staging tool when the CT scan fails to find evidence of T3, T4, or metastatic disease.
Institutions that favor neoadjuvant chemoradiotherapy for patients with locally advanced disease rely on endoscopic ultrasound
data to improve patient stratification.
In a study of peritoneal cancer (PC) diagnosis, investigators found that the administration of carbonated water for dual-time point
imaging may improve the accuracy of FDG PET/CT scanning for PC in patients previously diagnosed with colorectal cancer
(CRC).
Histologic Findings
Adenocarcinoma of the stomach constitutes 90-95% of all gastric malignancies. The second most common gastric malignancies
are lymphomas. Gastrointestinal stromal tumors formerly classified as either leiomyomas or leiomyosarcomas account for 2% of
gastric neoplasms (see Gastric Stromal Tumors). Carcinoids (1%), adenoacanthomas (1%), and squamous cell carcinomas (1%)
are the remaining tumor histologic types.
Adenocarcinoma of the stomach is subclassified according to histologic description as follows: tubular, papillary, mucinous, or
signet-ring cells, and undifferentiated lesions.
Pathology specimens are also classified by gross appearance. In general, researchers consider gastric cancers ulcerative,
polypoid, scirrhous (ie, diffuse linitis plastica), superficial spreading, multicentric, or Barrett ectopic adenocarcinoma.
Researchers also employ a variety of other classification schemes. The Lauren system classifies gastric cancer pathology as either
Type I (intestinal) or Type II (diffuse). An appealing feature of classifying patients according to the Lauren system is that the
descriptive pathologic entities have clinically relevant differences.
Intestinal, expansive, epidemic-type gastric cancer is associated with chronic atrophic gastritis, retained glandular structure, little
invasiveness, and a sharp margin. The pathologic presentation classified as epidemic by the Lauren system is associated with
most environmental risk factors, carries a better prognosis, and shows no familial history.
The second type, diffuse, infiltrative, endemic cancer, consists of scattered cell clusters with poor differentiation and dangerously
deceptive margins. Margins that appear clear to the operating surgeon and examining pathologist often are determined
retrospectively to be involved. The endemic-type tumor invades large areas of the stomach. This type of tumor is also not
recognizably influenced by environment or diet, is more virulent in women, and occurs more often in relatively young patients.
This pathologic entity is associated with genetic factors (such as E-cadherin), blood groups, and a family history of gastric
cancer.
In 2013, researchers identified a possible third type of gastric adenocarcinoma. In an analysis of 248 gastric tumors using
microarray-based gene-expression profiling, Lei et al found that this third subtype of gastric adenocarcinoma (which they termed
the "metabolic" subtype; the other 2 subtypes are mesenchymal and proliferative) preferentially responds to 5-fluorouracil (5-
FU). The researchers validated their findings in an independent set of 70 gastric tumors.
[20, 21]
They believe that the preferential
sensitivity of metabolic-subtype gastric cancers to 5-FU may be due to their significantly lower expression of thymidylate
synthase and dihydropyrimidine dehydrogenase relative to the other 2 subtypes.
4. Differential diagnosis
Chronic calculous cholecystitis
Pancreatic cancer
Esophageal cancer

5. Rule in rule out - at least five. And reasons why..
Chronic calculous cholecystitis
Rule in Rule out

Pancreatic Cancer
Rule in Rule out

Esophageal Cancer
Rule in Rule out

6. Anatomy, blood supply, venous drainage,
Blood supply
Right gastric artery
Left gastric artery
Right gastro omental artery
Left gastro omental artery
Short gastric arteries
Venous Drainage
Right gastric vein
Left gastric vein
Right gastro omental vein
Left gastro omental vein
Short gastric veins
Nerve
Celiac ganglia, vagus
Lymph
Celiac lymph nodes

7. Physiology

8. Main prob (pathophysio, etiology, sign and symptoms)

9. Diagnostic work ups


10. Treatment options ( procedure and possible complications)
Surgical Care
Type of surgery
In general, most surgeons in the United States perform a total gastrectomy (if required for negative margins), an
esophagogastrectomy for tumors of the cardia and gastroesophageal junction, and a subtotal gastrectomy for tumors of the distal
stomach.
A randomized trial comparing subtotal with total gastrectomy for distal gastric cancer revealed similar morbidity, mortality, and
5-year survival rates.
[26]

Because of the extensive lymphatic network around the stomach and the propensity for this tumor to extend microscopically,
traditional teaching is to attempt to maintain a 5-cm surgical margin proximally and distally to the primary lesion.
Lymph node dissection
The extent of the lymph node dissection is somewhat controversial.
Many studies demonstrate that nodal involvement indicates a poor prognosis, and more aggressive surgical approaches to attempt
to remove involved lymph nodes are gaining popularity.
Two randomized trials compared D1 (perigastric lymph nodes) with D2 (hepatic, left gastric, celiac, and splenic arteries, as well
as those in the splenic hilum) lymphadenectomy in patients who were treated for curative intent. In the largest of these trials,
postoperative morbidity (43% versus 25%) and mortality (10% versus 4%) were higher in the D2 group.
[27, 28]

Most critics argue that these studies were underpowered and overestimated benefit. In addition, a recent randomized trial found a
much lower rate of complications than those earlier trials. Degiuli et al reported complication rates of 17.9% and 12% with D2
and D1 dissections, respectivelya statistically insignificant difference and postoperative mortality rates of 2.2% and 3%,
respectively.
[29]

D2 dissections are recommended by the National Comprehensive Cancer Network over D1 dissections. A pancreas- and spleen-
preserving D2 lymphadenectomy is suggested, as it provides greater staging information, and may provide a survival benefit
while avoiding its excess morbidity when possible.
Outcome
The 5-year survival rate for a curative surgical resection ranges from 60-90% for patients with stage I, 30-50% for patients with
stage II disease, and 10-25% for patients with stage III disease.
Because these patients have a high likelihood of local and systemic relapse, some physicians offer adjuvant therapy.
D1 gastrectomy is associated with less anastomotic leaks, a lower postoperative complication rate, a lower reoperation rate,
decreased length of hospital stay, and a lower 30-day mortality rate. The 5-year survival rate in patients who underwent D1
gastrectomy was similar to the D2 cohort.
[30]

A study by Bang et al found that adjuvant capecitabine plus oxaliplatin treatment after curative D2 gastrectomy should be
considered among patients with operable gastric cancer; however, D2 surgeries are not common in the United States due to
morbidity concerns and a lack of level 1 evidence of a survival advantage.
[31]

A more recent study suggests that survival in advanced gastric cancer is also improved with an adjuvant chemotherapy regimen.
Data from the open-label randomized Capecitabine and Oxaliplatin Adjuvant Study in Stomach Cancer (CLASSIC) indicate that
after surgery for advanced gastric cancer, treatment with capecitabine and oxaliplatin (XELOX) cuts the risk of death by 34%
over 5 years, as compared with surgery alone.
[32, 33]

In the CLASSIC study, patients with stage II to IIIB gastric cancer who had undergone curative D2 gastrectomy were assigned to
adjuvant XELOX for 8 cycles or surgery alone. The XELOX regimen consisted of oral capecitabine (1000 mg/m twice daily on
days 1-14 of each cycle) plus intravenous oxaliplatin (130 mg/m on day 1 of each cycle) for 6 months.
[32, 33]

At 5 years , there was a 34% reduction in the risk of death with XELOX, as compared with surgery alone.
[32, 33]
The 5-year
overall survival rate was also better with XELOX (78% vs 69%), as well as the 5-year disease-free survival rate (68% with
XELOX and 53% without).