Tumor GIT

Fanny Indarto, dr., Sp.B

Ruang lingkup
 GIST
 Limfoma
 Ca Pankreas
 Polip kolon
 Ca colon
Gastrointestinal Stromal
Tumors
(GIST)

 Arise
from the interstitial cells of Cajal and
represent the most common type of
mesenchymal tumors of the GI tract.
 Since the landmark discovery of the role
of proto-oncogene tyrosine kinase
receptor CD117 mutations associated
with GIST in 1998 by Hirota et al, the
diagnosis has been significantly
facilitated.
Symptoms
 Bleeding from submucosal ulceration of
the tumor
 obstructive symptoms of gastric outlet
obstruction
 abdominal pain.
Site of involvement
 stomach (60%)
 small intestine (30%)
 other sites along the GI tract (colon,
esophagus) and extra GI tumors being
less.
 Generally,
GIST does not spread to the
lymphatic system.
Treatment
 Resectable GIST without evidence of
metastases is primary R0 surgical resection
with consideration of adjuvant targeted
therapy with imatinib mesylate after
analysis of tumor size, mitotic rate, and
location of the tumor.
 Imatinib is the first-line treatment
 Sunitinib is secondline therapy reserved for
imatinib-resistant tumors.
Gastric lymphoma

 Gastric lymphoma is an extranodal Non-

Hodgkin lymphoma defined by the
presence of the majority of the lymphoma
in the stomach with variable involvement
of the surrounding lymphatic drainage.
 Gastric lymphoma is the most common
site of GI lymphoma followed by small
intestine, ileocecum, and colon/rectum.
 Risk factors : celiac disease, H. pylori
infection, immunosuppression, human
immunodeficiency virus (HIV) or Epstein-
Barr virus (EBV), and inflammatory bowel
disease.
Symptoms
 Nonspecific
 fever,
nausea, vomiting, epigastric
abdominal pain, anorexia, unintentional
weight loss, night sweats, hematemesis,
and melena.
Diagnostic
 Contrast-enhanced CT, MRI, EGD
biopsies, EUS,and 18F-fluorodeoxyglucose
PET (18FDG-PET).
 The treatment of choice for DLBCL is
chemotherapy alone.
 Treatment of H. pylori with triple therapy
(amoxicillin or metronidazole,
clarithromycin, and proton pump
inhibitors) has produced complete
remission of MALT lymphomas and is
considered the first line treatment.
Pancreatic Cancer
 Overall, pancreatic cancer has the worst
prognosis of all malignancies with a 5-year
survival rate of only 6%.
 Pancreatic cancer is more common in the
elderly >60 years old. Pancreatic cancer is
more common in African Americans and
slightly more common in men than women.
 The risk of developing pancreatic cancer is
two to three times higher if a parent or sibling
had the disease.
Etiology
Genetic Environment
 K-ras
gene  Diabetic
mutation  Obesity
 Cigarrete smoking
 Chronic
pancreatitis history
 About two-thirds of pancreatic
adenocarcinomas arise within the head
or uncinate process of the pancreas; 15%
are in the body, and 10% in the tail, with
the remaining tumors demonstrating
diffuse involvement of the gland.
 Tumors in the pancreatic body and tail
are generally larger at the time of
diagnosis, and therefore, less commonly
resectable.
 Tumors in the head of the pancreas are
typically diagnosed earlier because they
cause obstructive jaundice.
 In patients with jaundice  USG.
 If bile duct dilation is not seen, hepatocellular
disease is likely.
 Demonstration of cholelithiasis and bile duct
dilation  ERCP.
 No gallstones, malignant obstruction of the
bile duct is likely  CT scan rather than ERCP.
 For patients suspected of having pancreatic
cancer who present without jaundice, a CT
scan should be the first test.
 Diagnostic laparoscopy with the use of US
is reported to improve the accuracy of
predicting resectability to about 98%.
Symptoms
 Jaundice and accompanying pruritus.
 Biliary obstruction  cholangitis,
coagulopathy, digestive symptoms, and
hepatocellular failure.
 Duodenal obstruction is usually a late
event & only about 20% of patients.
Treatment
 For patients with locally advanced
unresectable disease are treated with
chemotherapy and possibly radiation.
 Patients with Stage IV metastatic disease
are treated with systemic chemotherapy.
Polip
 Clinical term for any mucosal elevation.
 Polyps are further categorized along several
dimensions
1. Size
2. Character of their attachment to the bowel wall
(eg, sessile or pedunculated)
3. Cellular architecture (eg, adenomas, hyperplastic,
hamartomas, inflammatory) and histologic
appearance (eg, tubulous, tubulovillous, villous)
4. Progression from benign to malignant behavior
(eg, benign, dysplastic, cancer)
 The risk of malignant degeneration is related
to both the size and type of polyp.
 Tubular adenomas are only 5% of cases,
villous adenomas may up to 40%.Tubulovillous
adenomas are at intermediate risk (22%).
 Invasive carcinomas are rare in polyps smaller
than 1 cm. The risk of carcinoma in a polyp
larger than 2 cm is 35% to 50%.
 Although most neoplastic polyps do not
evolve to cancer, most colorectal
cancers originate as a polyp.
 It is this fact that forms the basis for
secondary prevention strategies to
eliminate colorectal cancer by targeting
the neoplastic polyp for removal before
malignancy develops.
 Polypsmay be pedunculated or sessile.
Most pedunculated polyps are amenable
to colonoscopic snare excision.
Hyperplastic polyps
 Extremely common in the colon.
 Are usually small (<5 mm) and show
histologic characteristics of hyperplasia
without any dysplasia.
 They are not considered premalignant,
but cannot be distinguished from
adenomatous polyps colonoscopically
and are therefore often removed.
Colon Cancer
 Colorectal cancer is the most common
malignancy in the gastrointestinal tract.
 The specific cause of colorectal cancer is
not known. However, a number of
genetic and environmental risk factors
have been associated with the disease.
Patophysiology
three major genetic pathways:
 the loss of heterozygosity (LOH;
chromosomal instability) pathway
 the microsatellite instability (MSI) pathway
 the CpG island methylation (CIMP;
serrated methylated) pathway.
adenoma-carcinoma
sequence sequence
Natural history
 From mucosa invades the bowel wall and
adjacent tissues.
 Tumors may become bulky and
circumferential, leading to colon obstruction.
 Regional lymph node involvement is the most
common form of spread of colorectal
carcinoma and usually precedes distant
metastasis or the development of
carcinomatosis
 In patients with a colon cancer,
synchronous colorectal cancers are
found in 5% to 10%, whereas about 10% to
20% of patients with a history of colorectal
cancer will develop metachronous
primary cancers in the large intestine.
Screening Colorectal Cancer
Carcinoembryonic Antigen
(CEA)
 a glycoprotein found in the embryonic endodermal epithelium.
 Elevated CEA levels in patients with primary colorectal cancer, in
patients with breast, lung, ovarian, prostate, liver, and pancreatic
cancer.
 Levels of CEA also may be elevated in benign conditions :
diverticulitis, peptic ulcer disease, bronchitis, liver abscess, and
alcoholic cirrhosis, especially in smokers and in elderly persons.
 Use of CEA level as a screening test for colorectal cancer is not
recommended.
 CEA levels may be useful if obtained preoperatively and
postoperatively in patients with a diagnosis of colorectal cancer.
 Preoperative elevation of CEA level is an indicator of poor
prognosis.
Symptoms
 are nonspecific.
 The classic first symptoms are a change in
bowel habits and rectal bleeding.
 Abdominal pain, bloating, and other signs of
obstruction typically occur with larger tumors
and suggest more advanced disease.
 Left-sided tumors are more likely to cause
obstruction than are right-sided tumors.
 Patients may be asymptomatic and/or
present with unexplained anemia, weight loss,
or poor appetite.
 The colon must be evaluated for synchronous
tumors, usually by colonoscopy.
 A chest/abdominal/pelvic CT scan should be
obtained to evaluate for distant metastases.
 Among patients with obstructive symptoms, a
water-soluble contrast study (Gastrografin
enema) may be useful for delineating the
degree of obstruction.
 Preoperative CEA is often obtained and may
be useful for postoperative follow-up.
Principles of surgery
 remove the primary tumor along with its
lymphovascular supply.
 Thepresence of synchronous cancers or
adenomas or a strong family history of
colorectal neoplasms  subtotal or total
colectomy should be considered.
 Metachronous tumors (a second primary
colon cancer) identified during follow-up
studies should be treated similarly.
Stage 4
 Methods such as colonic stenting for
obstructing lesions of the left colon.
 Diverting stoma or bypass procedure
 Hemorrhage in an unresectable tumor
can sometimes be controlled with
angiographic embolization.
 External beam radiation also has been
used for palliation.
Carcinoid appendix
 The finding of a firm, yellow, bulbar mass
in the appendix should raise the suspicion
of an appendiceal carcinoid. The
appendix is the most common site of
gastrointestinal carcinoid, followed by the
small bowel and rectum.
 Themajority of carcinoids are located in
the tip of the appendix.
 Treatment for tumors ≤1 cm is
appendectomy. For tumors larger than 1
to 2 cm located at the base, involving the
mesentery, or with lymph node
metastases, right hemicolectomy is
indicated.
Mucocele appendix
 is an obstructive dilatation by intraluminal
accumulation of mucoid material.
..
Mucoceles may be caused by one of
four processes: retention cysts, mucosal
hyperplasia, cystadenomas, and
cystadenocarcinomas
Symptoms
 nonspecific, and often incidental finding
at operation for acute appendicitis
Treatment
 Does not mandate performance of a right
hemicolectomy.
 The principles of surgery : resection of the
appendix, wide resection of the
mesoappendix to include all the
appendiceal lymph nodes, collection and
cytologic examination of all
intraperitoneal mucus, and careful
inspection of the base of the appendix.
Source
 Schwartz'sPrinciples of Surgery 10th Ed
 Maingotʼs Abdominal Operations, 11th ed.
 Thank You