2. 1. Carcinoma of stomach comprises more than 90%
of all gastric malignancies and is called ‘Captain
of men of death’.
2. More common in JAPAN
3. Incidence male: female = 2:1
4. Decreased incidence in western world
3. CA proximal stomach (common) young and
upper socio-economic group
CA distal stomach older and low socio-
economic group
Usually has a poor prognosis.
5. High salt diet
Food with more nitrosamine releases
polycyclic hydrocarbons.
Preserved food rich in nitrates and nitrites will be
converted to nitrosamine by GI bacteria.
Smoked foods, pickled raw vegetables
Decreases incidence Fruits and green leafy
vegetables rich in Vitamin C.
Smoking and alcohol
6. Highest JAPAN, CHINA, ITALY
Lowest US, UK , CANADA
Western countries More common site is
proximal stomach near OG junction.
Asian countries more common in distal
stomach.
Indian statistics South > North
7. H. PYLORI INFECTION (Cag A strain)
1. H.Pylori infection co-exist with Gastric
lymphomas (MALT type)
2. Seropositive for HP increases risk by -4
times.
Epstein Barr Virus (EBR Virus)
8. Familial – 10% mutation in e-cadherin gene in a
autosomal dominant pattern causes hereditary diffuse
gastric cancers.
Inactivation of p53 gene.
Over expression of growth factors
Mutations in bcl-2 gene
Seen more in people with A blood group.
HNPCC, Li Fraumeni syndrome
Mutation of H-ras oncogene and mutation in c-erb
B2 gene.
Monozygotic twins > Dizygotic twins
9. Gastric polyps, adenomatos polyps > 2cm
Chronic benign gastric ulcers (ulcer cancer of
stomach)
Stump carcinoma in patients that have
undergone partial gastrectomy.
Hypo or achlorhydria in atropic gastritis
Giant hyperplasia of gastric mucosal folds –
Menetrier’s disease
10. Pernicious anaemia – increases risk 6 times
Gastric remnant – 15 years after gastrectomy and
GJ.
Chronic gastritis (atropic, autoimmune),
intestinal metaplasia
1. Type A proximal gastric cancers
2. Type B Distal gastric cancers
Gastric dysplasia
Agamaglobulinemia – high risk (2-5%)
14. Risk depends on extent of metaplasia
H. Pylori is a major factor
Histologically:
Complete type: Glands are completely lined with
goblet cells and intestinal absorptive cells
indistinguishable form small bowel counterpart.
Incomplete type: contain columnar cells, goblet
cells without intestinal absorptive cells.
15. Giant hyperplasia of gastric mucosal folds –
Menetrier’s disease.
Adenomatos gastric polyps
Chronic atropic gastritis
Benign gastric ulcers risk depends on size of
ulcers
Stomach remnants (Stump carcinoma) – occurs
after Billroth II GJ or Vagotomy GJ. Common
site is close to stoma.
18. D – Diffuse type (33%)
Poor prognosis
Common family, A group, Young and female
Spread Lymphatic spread
Decreased E-cadherin with p53 and p16
inactivation
Types ulcerative and Linitis plastica
19. I –Intestinal type (53%)
Favourable prognosis
Common men, aged people, APC gene mutation
and involves p53 and p16.
Spread haematogenous route
Types polypoid and superficial
H. Pylori is common cause
Gastric mucosa is replaced by epithelium that
resembles small bowel mucosa.
O – Others [ Unclassified- 14%]
20. Early gastric carcinoma – CA limited to
mucosa and sub mucosa.
Grossly:
1. Type I – Polypoid type
2. Type II
o II a – Superficial elevated
o II b – Superficial flat
o II c – superficial depressed
3. Type III – ulcerated type
22. When CA crosses the basement membrane into
the muscularis propria or beyond.
Lymph nodes are not involved
25. Adenocarcinoma – most common
Papillary AC (most common)
Tubular AC
Mucinous AC
Signet-ring AC
Adeno squamous CA
Squamous cell CA – rare (occur near OG )
Undifferentiated CA
Others – Unclassified CA
32. Group I – Perigastric nodes
Group II – along the root of major vessels
Group III – at the root of superior mesenteric
artery and hepato duodenal ligament
Group IV – Distant lymph nodes
33. Liver – causing multiple liver secondaries
Present as multiple, hard nodules with
umblications due to central necrosis
34. Peritoneal seeding
Ascities
Krukenberg’s Tumour
Occurs without ascities
Retrograde lymphatic spread from stomach to ovary
Favoured by – absence of ascities, no denudation/
implantations/adhesions on the ovary surface.
Even early gastric cancer can cause this.
Rectal secondaries – sister Mary Joseph Umbilical
secondaries
38. Recent onset of loss of appetite and weight
Fatigue
Hypo chromic anaemia – iron deficiency (40%)
Upper abdominal pain
VGP with features of gastric outlet obstruction
VGP +ve
Ausculto-percussion test +ve
Surcussion splash +ve
39. Mass abdomen (pyloric mass is above umbilicus
and moves equally with respiration)
Dysphasia (mass in upper epigastrium)
Only mass abdomen – if arise from body of
stomach
40. Jaundice with palpable liver
Ascities
Anaemia, Cachexia
Hematemesis (15%) and melana
Perforation (occasionally)
Secondaries in liver (rare) and umbilicus – Sister
Mary Joseph nodules
Cutaneous secondaries
Krukenberg's tumour
41. +ve Troisier’s sign
+ve recto-vesical secondaries (Blumer shelf) on
per rectal examination
+ve Trousseau sign- migrating thrombophlebitis
(also found in CA-pancreas)
45. Hb% and Haematocrit
Ba-meal
Single contrast Ba study
Double contrast Ba study (more sensitive)
Gastroscopy with biopsy
ENDOSCOPY - gold standard
Endosonography – detect involvement of layers
of stomach and asses nodal involvement
46. Irregular filling defect
Loss of rugosity
Delayed emptying
Dilatation of stomach in CA –pylorus
Decreases stomach capacity – Linitis plastica
Margin of ulcer/lesion will projects into the
gastric lumen- Carmanns meniscus sign
47. USG abdomen – Liver secondaries, ascities, ovaries
CT scan – CT abdomen and CT thorax – see for
size, extent and infiltration of tumour and nodal
status
LFT and PT – secondaries of liver
FNAC – left supraclavicular LN
Laparoscopy – to stage the disease
Tetracycline fluorescence test
Tumour marker – CA 72-4 suggestive of relapse
Combined PET and CT – asses metabolic and
functional activity
49. Preoperative preparation
i. Correction of anaemia, nutrition, fluid and
electrolyte
ii. Asses cardiac, respiratory and renal status
iii. Stomach wash – normal saline
iv. Prophylactic antibiotics
v. Arrangement for Blood and FFP
50. In case of early growth – especially in pylorus
Lower radical gastrectomy with proximal 5cm
clearance.
Removal of:
Greater and lesser omentum
Lymph nodes
Spleen
Tail of pancreas
Later Bilroth II anstamosis
51. Growth seen in OG junction or upper part of
stomach.
Upper radical gastrectomy
Removal of:
Spleen
Both the omentum
LN
Later oesophagogastric anstamosis
53. Practiced in Japan
Done for early gastric cancer with size <2cm,
elevated, well differentiated tumours without
nodal disease.
Also done for protruded early gastric carcinoma
or ulcer-free depressed cancer which is well
demarcated.
54. IV injection of Hemato-porphyrin derivatives
photosensitiser is given initially; 48 hours later
laser light is delivered to tumour through
endoscope releases highly reactive singlet
oxygen which causes tumour necrosis.
56. Mictomycin (M)
5-Flurouracil (5-FU)
Cisplatin (C) , Epirubicin (E), Oxaliplatin (O)
FAM regimen 5-FU, Adriamycin, M
Neo-adjuvant therapy ECF – E C 5-FU
Bevacizumab – under trail
EOC – E O Capecitabine
EOX – E O X- Capecitabine
58. Given in stage III CA after radical gastrectomy.
Starts from 5th postoperative day to end of 2
years.
Inj IM – Picibanil
It is aimed at improving:
T cell count that is reduced
Reduce micro-metastasis
59. To palliate pain
To palliate vomiting
When there is bleeding
Improve appetite
Partial gastrectomy is the best method