AA.Gastric C II 06. ppt

DIA GNOSIS

GASTRIC ADENOCARCINOMA 

Diagnosis. I. 

* double - contrast radiographic examination 

(detecting small lesions by improving mucosal 

details) = (old) simplest diagnostic procedure 

for evaluation of pts with epigastric complaints; 

- stomach distended during radiographic 

examinations (decreased distensibility may be 

the only indication of diffuse infiltrative 

carcinoma)

DOUBLE - CONTRAST RADIOGRAPHIC EXAMINATION


Diagnosis. II. Gastric ulcers 

* early detected with radiography; 

- however, those appearing benign are a 

special problem = ? impossible to distinguish 

benign from malignant lesions (anatomic 

location of an ulcer, usually lessr curvature, is 

not in itself an indication of presence or 

absence of cancer)

GASTRIC 

ADENOCARCINOMA 

Diagnosis. III. 

Gastric ulcers 

* pooling of barium in a 

posterior ulcer that 

extends beyond lesser 

curve margin; 

- distortion of 

uninterrupted mucosal 

folds of stomach (drawn 

in towards ulcer)


Diagnosis. IV. Gastroscopy 

* gastroscopic biopsy and brush cytology 

mandatory for pts with a gastric ulcer; 

- to identify malignant gastric ulcers before they 

penetrate into surrounding tissues (rate of cure of 

lesions limited to mucosa or submucosa > 80%); 

- as deep as possible, due to submucosal location 

of lymphoid tumors (GC difficult to distinguish 

clinically or radiographically from gastric 

lymphomas) and gastrointestinal stromal tumors 

(GISTs)


Diagnosis. V. Gastroscopy 

* some physicians believe that gastroscopy is 

not mandatory if radiographic features are 

typically benign, if complete healing can be 

visualized by x - ray within 6 wks, and if a follow 

- up contrast radiograph shows normal 

appearance several mos later

GASTROSCOPY. I.

GASTROSCOPY. II.

GASTROSCOPY. III.

GASTROSCOPY. IV.

GASTROSCOPY. V.

ENDOSCOPIC 

ULTRASOUND. I. 

* positioning of 

ecographic endoscopic 

transducer [submucosal 

gastric mass (A) and 

duodenum (B)]; 

* water - filled balloon 

around transducer 

creates an acustic 

interfacies with area to 

be examined (with 

reducing air’s 

interference)

ENDOSCOPIC ULTRASOUND. II. 

* positioning of ecographic endoscopic transducer in gastric 

antrum; 

- normal gastric wall with alteranting dark (hipoecoic) and clear 

(hiperecoic) layers, histologically correlated (right) with mucosa, 

submucosa, muscularis propria and serosa or adventitia

ENDOSCOPIC ULTRASOUND. III. 

Adenocarcinoma of esophagus 

endoscopic US of esophageal adenocarcinoma: 

circumferential, thick tumor mass around transductor [on the 

left, invading adipose periesophageal tissue and (anechogen) 

discendent aorta]

ENDOSCOPIC ULTRASOUND. IV. 

Gastric lipoma 

gastric lipomas: endoscopy (left): smooth contour masses; 

endoscopic US (right): hypoechoic mass in submucosa 

(mucosa and muscularis propria are normal)

ENDOSCOPIC ULTRASOUND. V. 

Gastric cancer confined to mucosa

ENDOSCOPIC ULTRASOUND. VI. 

Gastric cancer penetrating through wall of stomach 

TU = gastric tumor; PV = portal vein; SV = splenic vein

ENDOSCOPIC ULTRASOUND. VII. 

Gastric cancer invading pancreas 

TU = gastric tumor; PV = portal vein; LN = lymph node

DISSEMINATION


Dissemination. I. 

* by direct extension through gastric wall to perigastric 

tissues (occasionally adhering to adjacent organs such 

as pancreas, colon or liver); 

- via lymphatics to intraabdominal (frequent) and 

supraclavicular lymph nodes (Troisier’ sign); 

- by seeding of peritoneal surfaces [metastatic 

nodules to ovary (Krukenberg's tumor), periumbilical 

region ("Sister Mary Joseph node") or peritoneal cul-desac 

(Blumer's shelf)]; 

- malignant ascites; 

- hematogenous spread (more frequently to liver)

GASTRIC 


Dissemination. II.


Dissemination. III. Bone marrow involvement

STAGING


TNM: PRIMARY TUMOR 

- TX: primary tumor cannot be assessed; 

- T0: no evidence of primary tumor; 

- Tis: carcinoma in situ = intraepithelial tumor without 

invasion of lamina propria; 

- T1: tumor invades lamina propria or submucosa; 

- T2: tumor invades muscularis propria or subserosa; 

- T3: tumor penetrates serosa (visceral peritoneum) 

without invading adjacent structures; 

- T4: tumor invades adjacent structures


TNM: PRIMARY TUMOR. I. 

- TX: primary tumor cannot be assessed; 

- T0: no evidence of primary tumor; 

- Tis: carcinoma in situ = intraepithelial tumor without invasion of 

lamina propria; 

- T1: tumor invades lamina propria or submucosa; 

- T2: tumor invades muscularis propria or subserosa* 

[* T2 = tumor penetrates muscularis propria with extension to 

gastrocolic or gastrohepatic ligaments or to greater or lesser 

omentum without perforation of visceral peritoneum covering 

these structures (with perforation of visceral peritoneum covering 

gastric ligaments or omentum, tumor is classified T3)]

TNM FOR GASTRIC ADENOCARCINOMA 

TNM: PRIMARY TUMOR. II. 

- T3: tumor penetrates serosa (visceral peritoneum) 

without invading adjacent structures**; 

- T4: tumor invades adjacent structures, including 

spleen, transverse colon, liver, diaphragm, pancreas, 

abdominal wall, adrenal gland, kidney, small intestine 

and retroperitoneum 

[** intramural extension to duodenum or esophagus 

is classified by depth of greatest invasion in any of 

these sites, including stomach]

TNM FOR GASTRIC ADENOCARCINOMA 

TNM: PRIMARY TUMOR. III. 

- Tis: carcinoma in situ = 

intraepithelial tumor without 

invasion of lamina propria; 

- T1: tumor invades lamina 

propria or submucosa; 

- T2: tumor invades muscularis 

propria or subserosa; 

- T3: tumor penetrates serosa 

(visceral peritoneum) without 

invading adjacent structures; 

- T4: tumor invades adjacent 

structures


TNM: REGIONAL LYMPH NODES (LN*) 

NX: regional LN not assessed; 

N0: no regional LN metastasis; 

N1: metastasis in 1 - 6 regional LN; 

N2: metastasis in 7 - 15 regional LN; 

N3: metastasis in > 15 regional LN; 

* = perigastric nodes (along lesser and greater curvatures) and 

nodes located along left gastric, common hepatic, splenic and celiac 

arteries (for pN, lymphadenectomy specimen will contain at least 15 

LN); 

- involvement of other intra - abdominal lymph nodes (e.g., 

hepatoduodenal, retropancreatic, mesenteric and para - aortic LN, 

classified as distant metastasis)


TNM: REGIONAL LYMPH NODES 

* regional lymph nodes: 

- N1 = perigastric (along lesser and greater curvatures); 

- N2 = along left gastric artery, and 

- N3 = along common hepatic, splenic and celiac arteries; 

* metastatic lymphnodes (= metastases): other intra - abdominal 

lymph nodes (e.g., hepatoduodenal, retropancreatic, mesenteric, 

and para - aortic LN)


Classification and anatomy of lymph node groups 

* N1 disease = involvement of 

perigastric LN along lesser or greater 

curvature (1 - 6) [1, right paracardial; 2, 

left paracardial; 3, lesser curvature; 4, 

greater curvature; 5, suprapyloric; 6, 

infrapyloric]; 

* N2 - N3 disease = involvement of LN 

along celiac axis (N2) and its 3 

branches (N3) (7 -11) [7, left gastric 

artery; 8, common hepatic artery; 9, 

celiac artery; 10, splenic hilus; 11, 

splenic artery]; 

* N4 disease = involvement of more 

distant LN (12 - 14) [12, hepatic 

pedicle; 13, retropancreatic; 14, 

mesenteric root; 15, middle colic 

artery; 16, para-aortic]


TNM: DISTANT METASTASIS (M) 

MX: distant metastasis cannot be assessed; 

M0: no distant metastasis 

M1: distant metastasis


AJCC stage subgrouping. I. 

Stage 0 

- Tis, N0, M0 

Stage IA 

- T1, N0, M0 

Stage IB 

- T1, N1, M0 

- T2, N0, M0 

Stage II 

- T1, N2, M0 

- T2, N1, M0 

- T3, N0, M0


AJCC stage subgrouping. II. 

Stage IIIA 

- T2, N2, M0 

- T3, N1, M0 

- T4, N0, M0 

Stage IIIB 

- T3, N2, M0 

Stage IV 

- T4, N1, M0 

- T1, N3, M0 

- T2, N3, M0 

- T3, N3, M0 

- T4, N2, M0 

- T4, N3, M0 

- any T, any N, M1

STAGING GASTRIC CANCER

TNM STAGING SYSTEM 

FOR GASTRIC CANCER

R0 = no residual tumor; R1 = microscopic residual tumor; 

R2 = macroscopic residual tumor

TREATMENT

SURGERY


Treatment. I. Surgery 

* surgical removal of complete tumor + 

adjacent lymph nodes = only chance for cure; 

- possible in < 30% of pts; 

* in general: 

- subtotal gastrectomy = treatment of choice 

for pts with distal GC; 

- total or near - total gastrectomy for more 

proximal tumors

GASTRIC 

CARCINOMA 

Surgery


Treatment. II. Surgery


Treatment. III. Total gastrectomy 

* with proximal cancers, all stomach is removed (total 

gastrectomy) and gullet is joined directly onto small bowel 

(Roux - en - Y reconstruction)


Treatment. IV. Total gastrectomy


Treatment. V. Esophagogastrectomy 

* left) with cancers near cardia, a part of gullet is also removed 

(esophagogastrectomy) and top portion of gullet is joined to small 

bowel (“Roux - en - Y” reconstruction); 

* right) sometimes, furthest third of stomach is kept and remaining 

oesophagus is joined onto remaining part of stomach


Treatment. VI. Partial gastrectomy (Billroth I and II) 

* for cancers at distal 

stomach (connecting with 

duodenum) → partial 

gastrectomy, with sparing the 

valve (cardiac sphincter) 

between esophagus and 

stomach; 

- 2 different types of 

operation, i.e., Billroth I (for 

very small tumors in lower 

part of stomach, near 

pylorus) and Billroth II


Treatment. VII. Partial gastrectomy (Billroth I) 

* partial gastectomy (Billroth I), for very small tumors in 

lower part of stomach (near pylorus) connecting with 

duodenum, with sparing valve (cardiac sphincter) 

between esophagus and stomach


Treatment. VIII. Partial gastrectomy (Billroth I)


Treatment. XI. Partial gastrectomy (Billroth II) 

* partial gastectomy (Billroth II), for major tumors in 

lower part of stomach (near pylorus) connecting with 

small bowel, still with sparing valve (cardiac sphincter) 

between esophagus and stomach

GASTRIC 


Treatment. XII. 

Partial gastrectomy 

(Billroth I & II)

GASTRIC 


Treatment. XIII. 

Complications of surgery. I. 

Dumping syndrome 

palpitations, diaphoresis, 

flushing, hunger (but early 

epigastric fullness), 

borborygmi, abdominal 

cramps, diarrhea

GASTRIC 


Treatment. XIV. 

Complications of surgery. II. 

Ulcer 

Gastrocolic fistula


Treatment. XV. Prognosis after surgery 

* adversely influenced by degree of tumor 

penetration into stomach wall, regional lymph 

node involvement, vascular invasion and 

abnormal DNA content (i.e., aneuploidy, 

occurring in most pts); 

- for < 30% of pts able to undergo a complete 

resection of GC, 5 - yr survival is 20% for distal 

tumors and < 10% for proximal tumors 

(recurrences occurs for ≥ 8 yrs after surgery)


Treatment. XVI. Prognosis after surgery 

* survival according 

with ploidy and S phase fraction


Treatment. XVII. 

* in absence of ascites or extensive hepatic or 

peritoneal metastases, even pts whose disease 

is believed incurable by surgery should be 

offered an attempt at resection of primary 

lesion (reduction of tumor bulk is best form of 

palliation, ↑ subsequent benefit of 

chemotherapy and / or radiation therapy, ? 

avoids “emergency” surgery)

RADIOTHERAPY


Treatment. XVIII. Radiotherapy 

* GC is a radioresistant tumor (= achieving 

adequate control of primary tumor requires 

doses of external beam radiation exceeding 

tolerance of surrounding structures, such as 

bowel mucosa and spinal cord); 

- palliation of pain = major role of radiation 

therapy in pts with GC

CHEMOTHERAPY


Treatment. XIX. 

Chemotherapy for advanced disease 

* combinations of cytotoxic drugs to pts with 

advanced GC reduces > 50% measurable tumor mass 

in 30 - 50% of cases ("partial response"), with significant 

clinical benefit; 

- drug combinations generally include 5 - FU 

(variously with doxorubicin, mitomycin - C, cisplatin, 

high doses of methotrexate, irinotecan and 

oxaliplatin); 

* despite response, complete disappearances of 

tumor masses uncommon, partial responses transient 

and overall impact of multidrug therapy on survival 

doubtful


Treatment. XXX. Adjuvant chemotherapy 

* prophylactic (i.e., adjuvant) chemotherapy 

following complete resection of GC (as a 

mean of eradicating clinically undetectable 

micrometastases and improving potential for 

cure) possibly ?unsuccessful: 

→ adjuvant treatment [as well as of 

preoperative ("neoadjuvant")] chemotherapy 

still investigational


Treatment. XXXI. Metanalysis of adjuvant chemotherapy


Treatment. XXXII. Adjuvant chemotherapy 

* no survival advantage over classic 5 - FU alone in pts 

randomized to either 5 - FU alone, or 5 - FU, doxorubicin and 

cisplatin or 5 - FU, doxorubicin and methyl CCNU with triazinate 

(Cullinan et al 1994)

RADIO - CHEMOTHERAPY


Treatment. XXXIII. Adjuvant radio - chemotherapy. I. 

* radiation therapy alone after a complete 

resection does not prolong survival; 

- however, survival is prolonged when 5 - 

fluorouracil (5 - FU) is given in combination 

with radiation therapy (5 - FU functions as a 

radiosensitizer?)


Treatment. XXXIV. 

Adjuvant radio - chemotherapy. II. 

Immagine 4


Treatment. XXXV. 

Adjuvant 

radio - chemotherapy. III. 

irradiation fields


XXXVI. Major toxicities (≥ G3) of adjuvant 

radio - chemotherapy. IV. 

* hematologic (54%); 

* GI (33%); 

* flu - like (9%); 

* infection (6%); 

* neurological (4%); 

* cardiovascular (4%); 

* pain (3%); 

* hepatic (1%), respiratory (1%) & skin (1%)


Treatment. XXXVII. 

Adjuvant 

radio-chemotherapy. V. 

local failures 

in surrounding 

organs or tissues; 

* = lung metastases; 

+ = liver metastases

GASTRIC LYMPHOMA

GASTRIC LYMPHOMA 

* < 15% of gastric 

malignancies and 

2% of all lymphomas; 

- however, stomach 

is most frequent 

extranodal location 

for lymphoma, and 

- gastric lymphoma 

↑ in frequency during 

the past 20 yrs


* infection with H. pylori (also associated with 

development of GC) ↑ risk for gastric 

lymphoma [especially mucosa - associated 

lymphoid tissue (MALT) lymphomas)


Clinical and radiologic features 

* difficult to distinguish from GC: both 

- in 6th decade of life; 

- epigastric pain, early satiety, and generalized 

fatigue; 

- at contrast radiographs, usually ulceration with a 

ragged, thickened mucosal pattern (less frequently, 

bulky ulcerated lesion localized in corpus or antrum 

or a diffuse process spreading throughout entire 

gastric submucosa)


Diagnosis 

* by deep biopsy at time of gastroscopy (or at 

laparotomy); 

- usually, B - cell non - Hodgkin's lymphoma; 

- from well - differentiated, superficial processes 

(mucosa - associated lymphoid tissue, MALT) to 

high - grade, large cell lymphomas; 

- initially spreads to regional lymph nodes (often 

to Waldeyer's ring) and may disseminate; 

- staged like other lymphomas

C 

D 

GASTRIC MALT LYMPHOMA 

Diagnosis 

C) cytokeratin+ cells, lympho - 

epithelial lesions and monocytoid 

infiltrate (not neoplastic); 

D) neoplastic large cells expressing 

mainly B cell marker CD20; 

E) proliferative rate by Ki67 (MIB1) 

E


Treatment. I. 

* need for a correct diagnosis because 

gastric lymphoma is a far more treatable than 

GC; 

- antibiotic treatment to eradicate H. pylori 

infection → regression of ~ 50% of gastric MALT 

lymphomas (= to be considered before 

surgery, radiation therapy or chemotherapy)


Treatment. II. 

* chemotherapy alone largely substitutes 

surgery in pts with CT evidence of nodal 

involvement or more widespread disease


Treatment. III. 

* in pts with localized high - grade NHL 

(subtotal gastrectomy followed by) 

combination chemotherapy allows 5 - yr 

survival rates of 40 - 60%; 

- questioned radiation therapy to abdomen 

following surgical resection (most recurrences 

develop at sites distant from epigastrium = 

outside radiation treatment fields)

AA.Gastric C II 06. ppt

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