CARCINOMA STOMACH

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*Image via Bing STOMACH & DUODENUM

ANATOMY:

ANATOMY IN ADULT LIFE, STOMACH LOCATED T10 AND L3 VERTEBRAL SEGMENT CAN BE DIVIDED INTO ANATOMIC REGIONS BASED ON EXTERNAL LANDMARKS 4 REGIONS CARDIA FUNDUS CORPUS (BODY) ANTRUM

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Anatomy:

Anatomy CARDIA- REGION JUST DISTAL TO THE GE JUNCTION FUNDUS- PORTION ABOVE AND TO THE LEFT OF THE GE JUNCTION

Anatomy:

Anatomy CORPUS- REGION BETWEEN FUNDUS AND ANTRUM MARGIN NOT DISTINCTLY EXTERNAL, HAS ARBITRARY BORDERS ANTRUM- BOUNDED DISTALLY BY THE PYLORUS WHICH CAN BE APPRECIATED BY PALPATION OF A THICKENED RING OF SMOOTH MUSCLE

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*Image via Bing CROSS SECTION OF STOMACH

Anatomy:

Anatomy POSITION OF THE STOMACH VARIES WITH BODY HABITUS IN GENERAL- IT IS FIXED AT TWO POINTS PROXIMALLY AT THE GE JUCTION DISTALLY BY THE RETROPERITONEAL DUODENUM

Anatomy:

Anatomy ANTERIOR- IN CONTACT WITH LEFT HEMI-DIAPHRAGM, LEFT LOBE AND ANTERIOR SEGMENT OF RIGHT LOBE OF THE LIVER AND THE ANTERIOR PARIETAL SURFACE OF THE ABDOMINAL WALL POSTERIOR- LEFT DIAPHRAGM, LEFT KIDNEY, LEFT ADRENAL GLAND, AND NECK, TAIL AND BODY OF PANCREAS THE GREATER CURVATURE IS NEAR THE TRANSVERSE COLON AND TRANSVERSE COLON MESENTERY THE CONCAVITY OF THE SPLEEN CONTACTS THE LEFT LATERAL PORTION OF THE STOMACH

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BLOOD SUPPLY OF STOMACH:

BLOOD SUPPLY OF STOMACH BLOOD SUPPLY OF STOMACH ARISES FROM COELIAC AXIS LEFT GASTRIC ARTERY COMMON HEPATIC ARTERY SPLENIC ARTERY SPLENIC ARTERY GIVES SHORT GASTRIC LEFT GASTRO EPIPLOIC COMMON HEPATIC ARTERY GIVES RIGHT GASTRIC A.& GASTRO DUODENAL A. GASTRODUODENAL ARTERY GIVES RT. GASTROEPIPLOIC ART.

VASCULATURE:

VASCULATURE

VASCULATURE:

VASCULATURE WELL VASCULARIZED ORGAN ARTERIAL FLOW MAINLY DERIVED FROM CELIAC ARTERY 3 BRANCHES LEFT GASTRIC ARTERY SUPPLIES THE CARDIA OF THE STOMACH AND DISTAL ESOPHAGUS SPLENIC ARTERY GIVES RISE TO 2 BRANCHES WHICH HELP SUPPLY THE GREATER CURVATURE OF THE STOMACH LEFT GASTROEPIPLOIC SHORT GASTRIC ARTERIES COMMON HEPATIC OR PROPER HEPATIC ARTERY 2 MAJOR BRANCHES RIGHT GASTRIC- SUPPLES A PORTION OF THE LESSER CURVATURE GASTRODUODENAL ARTERY -GIVES RISE TO RIGHT GASTROEPIPLOIC ARTERY -HELPS SUPPLY GREATER CURVATURE IN CONJUNCTION WITH LEFT GASTROEPIPLOIC ARTERY

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Anatomy:

Anatomy VENOUS DRAINAGE PARALLELS ARTERIAL SUPPLY LYMPHATIC DRAINAGE LYMPH FROM THE PROXIMAL PORTION OF THE STOMACH DRAINS ALONG THE LESSER CURVATURE FIRST DRAINS INTO SUPERIOR GASTRIC LYMPH NODES SURROUNDING THE LEFT GASTRIC ARTERY DISTAL PORTION OF LESSER CURVATURE DRAINS THROUGH THE SUPRAPYLORIC NODES PROXIMAL PORTION OF THE GREATER CURVATURE IS SUPPLIED BY THE LYMPHATIC VESSELS THAT TRAVERSE THE PANCREATICOSPLENIC NODES ANTRAL PORTION OF THE GREATER CURVATURE DRAINS INTO THE SUBPYLORIC AND OMENTAL NODAL GROUPS IN GENERAL- THE LYMPHATIC DRAINAGE OF THE HUMAN STOMACH, LIKE ITS BLOOD SUPPLY, EXHIBITS EXTENSIVE INTRAMURAL RAMIFICATIONS AND A NUMBER OF EXTRAMURAL COMMUNICATIONS. THEREFORE SPREAD BEYOND IS OFTEN BEYOND REGION OF ORIGIN AT A DISTANCE FROM THE PRIMARY LYMPHATIC ZONE

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Anatomy:

Anatomy NERVE SUPPLY LEFT AND RIGHT VAGUS NERVES DESCEND PARALLEL TO THE ESOPHAGUS WITHIN THE THORAX BEFORE FORMING A PERI-ESOPHAGEAL PLEXUS BETWEEN THE TRACHEAL BIFURCATION AND THE DIAPHRAGM FROM THIS PLEXUS, TWO VAGAL TRUNKS COALESCE BEFORE PASSING THROUGH THE ESOPHAGEAL HIATUS OF THE DIAPHRAGM

Anatomy:

Anatomy NERVELEFT (ANTERIOR) VAGUS LEFT OF THE ESOPHAGUS BRANCHES HEPATIC BRANCH SUPPLIES LIVER AND BILIARY TRACT ANTERIOR GASTRIC OR ANT. NERVE OF LATARGET

Anatomy:

Anatomy RIGHT (POSTERIOR) VAGUS NERVE RIGHT OF THE ESOPHAGUS BRANCHES CELIAC POSTERIOR LATARGET INNERVATES POSTERIOR GASTRIC WALL

Anatomy:

Anatomy PARASYMPATHETIC INNERVATION OF STOMACH- VAGUS NERVE 90% OF FIBER IN VAGAL TRUNK IS AFFERENT (INFO TRANSMITTING FROM STOMACH TO CNS) SYMPATHETIC INNERVATION OF STOMACH- SPLANCHNIC NERVE DERIVED FROM SPINAL SEGEMENT T5-T10

Anatomy:

Anatomy MICROSCOPIC ANATOMY GLANDULAR PORTIONS OF STOMACH LINED BY SIMPLE COLUMNAR EPITHELIUM THIS LUMINAL SURFACE IS INTERRUPTED AT INTERVALS BY GASTRIC PITS OPENING INTO THESE GASTRIC PITS ARE ONE OR MORE GASTRIC GLANDS THAT HAVE FUNCTIONAL SIGNIFICANCE MUCOSA HAS THREE TYPES OF GASTRIC GLANDS -CARDIAC -OXYNTIC -ANTRAL

Microscopic Anatomy:

Microscopic Anatomy CARDIAC GLANDS LOCATION- CARDIA CONTAIN MUCOUS FUNCTION- SECRETE MUCOUS (PROVIDES A PROTECTIVE COAT FOR LINING OF STOMACH) OXYNTIC GLANDS MOST DISTINCTIVE FEATURE OF THE STOMACH LOCATION- FUNDUS AND CORPUS CONTAINS MANY CELL TYPES

Microscopic Anatomy:

Microscopic Anatomy PARIETAL CELLS LOCATION- NECK OF GASTRIC PIT STIMULATED BY ACH, HISTAMINE AND GASTRIN SECRETES HCL + INTRINSIC FACTOR CHIEF CELLS LOCATION- BASE OF GASTRIC PIT STIMULUS- VAGAL SECRETES PEPSINOGEN (EVENTUALLY LEADS TO PEPSIN- DIGESTIVE ENZYME)

Microscopic Anatomy:

Microscopic Anatomy ANTRAL GLANDS GASTRIN CELLS LOCATION- MUCOSA OF DISTAL STOMACH STIMULUS- AMINO ACIDS SECRETION- GASTRIN (STIMULATES HCL PRODUCTION BY WAY OF PARIETAL CELLS) SOMATOSTATIN LOCATION- MUCOSA OF DISTAL STOMACH + DUODENUM STIMULUS- HCL OR LOW PH IN DUODENUM ACTIONS- INHIBITS GASTRIC EMPTYING, PANCREATIC SECRETIONS, AND GALLBLADDER CONTRACTION

Physiology:

Physiology THE STOMACH CONTAINS A NUMBER OF BIOLOGICALLY ACTIVE PEPTIDES IN NERVES AND ENDOCRINE CELLS EX. GASTRIN, SOMATOSTATIN, VASOACTIVE INTESTINAL PEPTIDE (VIP), SUBSTANCE P, AND GLUCAGON, ETC THE TWO PEPTIDES OF GREATEST IMPORTANCE TO HUMAN DISEASE AND CLINICAL SURGERY ARE GASTRIN SOMATOSTATIN

Physiology:

Physiology GASTRIN MOST IMPORTANT STIMULUS IS A MEAL AMINO ACIDS THAT RESULTS FROM PROTEOLYSIS FAT AND CARBOHYDRATES ARE NOT STIMULI FOR GASTRIN SECRETION GASTRIC DISTENTION THAT OCCURS FROM A MEAL WILL STIMULATE CHOLINERGIC NEURONS THEREBY RELEASING GASTRIN GASTRIN WILL THEN PROMPT PARIETAL CELL TO SECRETE HCL ONCE GASTRIC DISTENTION DIMINISHES, VIP-CONTAINING NEURONS ARE ACTIVATED CAUSING STIMULATION OF SOMATOSTATIN, THUS ATTENUATING GASTRIN SECRETION OVERALL, A LUMEN PH >3.0 WILL POTENTIATE GASTRIN RELEASE, WHEREAS A PH <3.0 WILL INHIBIT ITS RELEASE

Physiology:

Physiology Somatostain Like Gastrin, plays an integral role in gastric physiology Also, used for important therapeutic applications in treatment of digestive diseases Main stimulus is a low or acidic (<3.0)luminal pH Many peptides have shown to release somatostatin Ex. Secretin, Cholecystokinin and gastrin In contrast, stimulation of Vagal nerves along with cholinergic neurons inhibit somatostatin Overall, the most important gastric function of somatostatin is to regulate acid secretion and gastrin release

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Gastric Acid Secretion:

Gastric Acid Secretion Basolateral membrane of the parietal cell contains specific receptors for the three major stimulants of acid production Histamine Gastrin Acetylcholine Each stimulant has its own 2 nd messenger system which allows for stimulation of the parietal cell

Gastric Acid Secretion:

Gastric Acid Secretion Humans normally secrete 2 to 5 mEq/h of HCl in the fasting state, constituting basal acid secretion Both Vagal tone and ambient Histamine secretion are presumed to regulate basal acid secretion Gastrin is not thought to play a role in basal acid secretion Therefore, a Vagotomy or use of H2 blockers (ex. Cimetidine) will decrease basal acid production

Gastric Acid Secretion:

Gastric Acid Secretion Stimulated acid secretion begins with Cephalic phase Thought, sight or smell of food stimulates acid secretion Mediated by Vagal stimulation Vagal discharge Directs the cholinergic mechanism for stimulation Can be inhibited by Atropine (anticholinergic) Inhibits release of somatostatin Vagal effects inhibit tonic inhibition that is provided by somatostatin

Gastric Acid Secretion:

Gastric Acid Secretion Gastric Phase Begins when food enters the stomach The following are responsible for stimulation of acid secretion Presence of partially hydrolyzed food constituents Gastric distention Gastrin is the most important mediator of this phase Ends when Antral muscosa is exposed to acid When luminal pH is <2.0 in the antrum, gastrin release stops Somatostatin release is increased Entry of digestive products into the intestine begins the intestinal-phase inhibition of gastric acid secretion

Gastric Acid Secretion:

Gastric Acid Secretion Intestinal Phase Also, releases HCl by way of Gastrin Releases secretin to inhibit Gastrin which ultimately decreases Acid production

Other Factors:

Other Factors Pepsin Secreted from gastric chief cells Contributes to the overall coordination of the digestive process Main function is to initiate protein digestion, usually is incomplete Partially hydrolyzed protein by pepsin are important signals for release of Gastrin Cholecystokinin

Other Factors:

Other Factors Intrinsic Factor (IF) Located in the parietal cells (oxyntic gland) Main function is to absorb cobalamin (Vitamin B12) form ileal mucosa and then transported to the liver Secretion of IF is similar to acid secretion stimulated Ach Histamine Gastrin

Other Factors:

Other Factors Bicarbonate Secreted from the gastric mucosa Theory is that bicarbonate is secreted to maintain a neutral pH at the mucosal surface, even if acidic in lumen Cholinergic agonist, vagal nerve stimulation have been shown to increase gastric bicarbonate production

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Background:

Background Second most common cancer-related death. Korea, Japan, China, Taiwan high rates. 22,000 diagnosed annually in US. 14 th most common cancer. Difficult to cure, as advanced disease. Most die of recurrent disease even after resection for cure.

CARCINOMA STOMACH:

CARCINOMA STOMACH DR.M.RAVICHANDRA,M.S

Anatomy:

Anatomy Stomach begins at GE junction, ends at duodenum. 3 parts- uppermost is cardia, largest part in middle is body, the last part is pylorus. Cardia contains mucin producing cells. Fundus or body mucoid cells, chief cells, parietal cells. Pylorus has mucin producing cells.

Anatomy:

Anatomy Five layers: Mucosa, submucosa, muscular layer, subserosal layer, serosal layer. Peritoneum of greater sac covers anterior surface A portion of lesser sac drapes posteriorly over stomach. The GE junction has limited serosal covering.

Frequency:

Frequency US: seventh leading cause of cancer deaths, with 22,000 diagnosed yearly, and 14,000 deaths. Internationally: second most common cancer. Tremendous geographic variation, with highest death rates in Chile, Japan, and former USSR.

Race:

Race Higher in Asian countries. Japanese detect patients at very early stage, patients appear to do quite well.

Etiology:

Etiology Diet H. Pylori Previous stomach surgery Pernicious anemia Polyps( rarely a precursor) Atrophic gastritis Radiation, genetics

Diet:

Diet Certain diets are implicated. Rich in pickled vegetables, salted fish, excessive dietary salt, smoked meats. A diet that includes fruits and vegetables rich in vitamin C may have a protective effect. Excessive amounts of nitrates are converted to nitites and nitroseamine which are potential carcinogens.

Helicobacter :

Helicobacter Implicated as precursor of gastric cancer. H. Pylori associated with atrophic gastritis, and patients with a history of prolonged gastritis have a 6-fold increase in risk. Particularly true of tumors of antrum, body, and fundus of stomach, but not in cardia.

Previous Surgery:

Previous Surgery Peptic ulcer surgery- Partial gastrectomy, GastroJejunostomy, Pyloroplasty Implicated as risk factor, the rational being that previous gastric surgery alters normal pH of stomach as well as bile reflux gastritis Polyps may be premalignant.

Genetic Factors:

Genetic Factors Poorly understood Some familial aggregation exists Mutation of H- ras oncogene and over expression of c-erb –B2 genes APC – Familial Polyposis P53 suppressor gene HNPCC

Sites of distribution:

Sites of distribution The site of the lesion is classified on basis of relationship to long axis of stomach. CARDIA-21% FUNDUS-2% BODY-23% PYLORUS-47%

History:

History Early disease has no symptoms, some patients with incidental complaints get an early diagnosis. If symptoms, it reflects advanced disease; These may include indigestion, nausea, dysphagia, early satiety, anorexia, weight loss.

History:

History Late complications include: pleural effusions, peritoneal effusions, Gastric Outlet Obstruction, Gastro Esophageal obstruction, Small Bowel Obstruction, bleeding, jaundice, cachexia.

Physical examination:

Physical examination All physical signs are late events. Too late for curative procedures. Palpable stomach with succussion splash, hepatomegaly, Virchow nodes, sister Mary Joseph nodes, Blumer shelf, weight loss, pallor from bleeding and anemia.

Laboratory:

Laboratory Assists in determining optimal therapy. CBC identifies anemia, with may be caused by bleeding, liver dysfunction, or poor nutrition. 30% have anemia. Electrolyte panels and LFTs are also essential to better characterize patients clinical state.

Imaging Studies:

Imaging Studies EGD: safe, simple, providing a permanent color photographic record. Obtains tissue for diagnosis. UGI: detects large tumors, but only occasionally detects extension into esophagus or duodenum, especially if small or submucosal.

Imaging Studies:

Imaging Studies CXR: done to evaluate for metastases. CT scan or MRI of chest, abdomen, pelvis: evaluate local disease process, and areas of spread. Some tumors are deemed unresectable based on the testing. Accurately predicts stage 66-77%. Poor nodal status prediction.

Endoscopic Ultrasound:

Endoscopic Ultrasound Endoscopic ultrasound: becoming extremely useful as a staging tool, when CT fails to show T3, T4, or metastatic disease. Used with neoadjuvant chemo to stratify pts Can achieve resolution of 0.1 mm. Cannot reliably distinguish between tumor and fibrosis. Overall staging accuracy of 75% Poor for T2 lesions (38%) Better for T1(80%), T3 (90%)

Histology:

Histology Adenocarcinoma 95% Lymphomas 2% Carcinoids 1% Adenocathomas 1% Squamous cell 1%

Histology:

Histology Adenocarcinoma is classified according to the most unfavorable microscopic element present: tubular, papillary, mucinous, signet-ring cells. Also identified by gross appearance: ulcerative, polypoid, scirrous, superficial spreading, multicentric, or Barrett ectopic. Variety of other schemes: Borrmann, Lauren.

Lauren System:

Lauren System Type I- intestinal gastric cancer, arises intestinal metaplasia. -forms polypoid tumour or ulcer Type II- Diffuse gastric cancer- infiltarting in stomach wall without producing obvious mass lesion

Macroscopic types:

Macroscopic types Proliferative type- bulky, cauliflower like Ulcerative type- the most type, Mc Pylorus antrum region towards lesser curvature. Colloid or mucoid type- rare variety, massive tumor of gelatinous appearance. Cancer cells line the accumulation of colloid. Linitis plastica- also a rare variety.tm cells infiltrate the sub-mucosa and subserosa and muscle coat extensively without protuding into the lumen of the stomach. Proliferation of fibrous tissue in the submucosa giving mother of pearl appearance. Localised –involves usually pylorus region generalized.(whole stomach ios contracted and rigid)

Staging:

Staging Primary tumor Tx- cannot be assessed T0- no evidence Tis- carcinoma in situ, no invasion of lamina T1- invades lamina propria or submucosa T2- invades muscularis or subserosa T3- penetrates serosa, no adjacent structure T4- invades adjacent structures

Regional Lymph Nodes:

Regional Lymph Nodes NX- cannot be assessed N0- no nodes N1- mets in 1-6 regional nodes N2- mets in 7-15 regional nodes N3- mets in more than 15 regional nodes

Distant Metastases:

Distant Metastases MX- cannot be assessed M0- no distant metastases M1-distant metastases

Early gastric cancer:

Early gastric cancer Gastic cancer confines to mucosa and submucosa irrespective of Lymph node status JAPANESE CLASSIFICATION OF EARLY GASTRIC CANCER Type I,II, a),b),c) III, Advanced Gastric Cancer- beyond submucosa coat and involves Muscularis propria Bormann’s classification Type I to IV

Prognostic Features:

Prognostic Features Depth of invasion through gastric wall, presence or absence of regional lymph node involvement The greater number of positive nodes, the greater the likelihood of local or systemic failure postoperatively

Spread Patterns:

Spread Patterns Directly, via lymphatics, or hematogenously Direct extension into omentum, pancreas, diaphragm, transverse colon, and duodenum. If lesion extends beyond wall to a free peritoneal surface, peritoneal involvement is frequent.

Spread Patterns:

Spread Patterns The visible gross lesion frequently underestimates true extent. Abundant lymphatic channels in submucosal and subserosal layers allow for easy spread. The submucosal plexus is prominent in esophagus, the subserosal plexus prominent in duodenum, which allows for proximal and distal spread. Liver mets common, from hematogenous spread.

Laparoscopy:

Laparoscopy Inspect peritoneal surfaces, liver surface. Identification of advanced disease avoids non-therapeutic laparotomy in 25%. Patients with small volume metastases in peritoneum or liver have a life expectancy of 3-9 months, thus rarely benefit from palliative resection.

Lymph Node Dissection:

Lymph Node Dissection AJCC: number rather than location of LN is prognostic. Extent of dissection controversial. Nodal involvement indicates poor prognosis, and more aggressive approaches to remove them are taking favor. Ongoing trials regarding this in Europe. Critics argue that the apparent benefit associated with extended LND reflects stage migration (each LN is reviewed more carefully).

Residual Disease R Status:

Residual Disease R Status Tumor status following resection. Assigned based on pathology of margins. R0- no residual gross or microscopic disease. R1- microscopic disease only. R2- gross residual disease. Long term survival only in R0 resection.

“D” Nomenclature:

“D” Nomenclature Describes extent of resection and lymphadenectomy. D1- removes all nodes within 3cm of tumor. D2- D1 plus hepatic, splenic, celiac, and left gastric nodes. D3- D2 plus omentectomy , splenectomy , distal pancreatectomy , clearance of porta hepatis nodes. Current standards include a D1 dissection only.

Type of Surgery:

Type of Surgery TOTAL GASTRECTOMY ( if required for negative margins), ESOPHAGOGASTRECTOMY for tumors of the cardia and GE junction, SUBTOTAL GASTRECTOMY for tumors of the distal stomach. Extensive lymphatics require 5cm margin.

Outcome:

Outcome 5-year survival for a curative resection is 30-50% for stage II disease, 10-25% for stage III disease. Adjuvant therapy because of high incidence of local and systemic failure.

Complications:

Complications Mortality 1-2% Anastamotic leak, bleeding, ileus, transit failure, cholecystitis, pancreatitis, pulmonary infections, and thromboembolism. Late complications include dumping syndrome, vitamin B-12 deficiency, reflux esophagitis, osteoporosis.

Adjuvant Therapy:

Adjuvant Therapy Rationale is to provide additional loco-regional control. Radiotherapy- studies show improved survival, lower rates of local recurrence when compared to surgery alone. In unresectable patients, higher 4 year survival with mutimodal tx, in comparison to chemo alone.

Chemotherapy:

Chemotherapy Numerous randomized clinical trials comparing combination chemotherapy in the adjuvant setting to surgery alone did not demonstrate a consistent survival benefit. The most widely used regimen is 5-FU, doxorubicin, and mitomycin-c. The addition of leukovorin did not increase response rates.

Advanced Unresectable Disease:

Advanced Unresectable Disease Surgery is for palliation, pain, allowing oral intake Radiation provides relief from bleeding, obstruction and pain in 50-75%. Median duration of palliation is 4-18 months

Tumour markers:

Tumour markers CEA CA 19-9 CA 50 CA 12-5 CA 72-4- MOST IMPORTANT

Thank you :

Thank you

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