A complete exam oriented slide on carcinoma stomach based on SRB text book of surgery.

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%)

11.  Radiation exposure
 Occupational – Rubber and coal workers
 Substance exposure  Zn, Pb, Talc, asbestos

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.

17.  Cauliflower type
 Ulcerative type
 Leather bottle (Linitis plastica)

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

24.  Expanding – Favourable prognosis
 Infiltrative – Poor prognosis

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

27.  Localised
 Intermediate
 Infilterating

28. Pre pyloric
and pyloric
region ( 65%)
Body (25%)
Fundus, OG
junction

30.  Horizontal sub mucosal spread (along stomach
wall)
 Vertical spread by invasion into adjacent
structures – Pancreas, Liver, Colon, Mesocolon

31.  Lymph nodes involved
 Sub-pyloric
 Gastric
 Pancreato-duodenal
 Splenic
 Coeliac
 Aortic
 Left supraclavicular (Virchow’s LN) – Troisier sign
 Retrograde spread – mesenteric LN of small bowel

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

36. 1. Confined to mucosa/muscularis propria
2. Muscularis/ serosal involvement
3. Nodal spread
4. Types
4a – Residual disease
4b – metastatic disease

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)

42.  Gastritis
 Pancreatic mass – carcinoma
 Transverse colon mass – carcinoma
 Acid peptic disease – Pyloric stenosis

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

52.  When growth is in body or Linitis plastica

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

57.  Postoperative radiotherapy with chemotherapy
using 5-FU and leucovorin is the standard
adjuvant therapy.

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

60.  Palliative partial gastrectomy
 Palliative anterior gastro-jejunostomy with
jejuno-jejunostomy
 Endoscopic stenting or dilatation
 Laser decanalisation
 Palliative chemotherapy – FAM regimen

61.  Early or advanced
 Histological grading
 Staging
 Gross types
 Lymph node involvement
 Liver secondaries
 Serosal involvement – important factor
 Intestinal type – better prognosis than diffuse
 Ascites
 Response to treatment