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Carcinoma stomach
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
 CA proximal stomach (common)  young and
upper socio-economic group
 CA distal stomach  older and low socio-
economic group
 Usually has a poor prognosis.
Carcinoma stomach
 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
 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
 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)
 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
 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
 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%)
 Radiation exposure
 Occupational – Rubber and coal workers
 Substance exposure  Zn, Pb, Talc, asbestos
Carcinoma stomach
Carcinoma stomach
 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.
 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.
Carcinoma stomach
 Cauliflower type
 Ulcerative type
 Leather bottle (Linitis plastica)
 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
 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%]
 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
Carcinoma stomach
 When CA crosses the basement membrane into
the muscularis propria or beyond.
 Lymph nodes are not involved
Carcinoma stomach
 Expanding – Favourable prognosis
 Infiltrative – Poor prognosis
 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
Carcinoma stomach
 Localised
 Intermediate
 Infilterating
Pre pyloric
and pyloric
region ( 65%)
Body (25%)
Fundus, OG
junction
Carcinoma stomach
 Horizontal sub mucosal spread (along stomach
wall)
 Vertical spread by invasion into adjacent
structures – Pancreas, Liver, Colon, Mesocolon
 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
 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
 Liver – causing multiple liver secondaries
 Present as multiple, hard nodules with
umblications due to central necrosis
 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
Carcinoma stomach
1. Confined to mucosa/muscularis propria
2. Muscularis/ serosal involvement
3. Nodal spread
4. Types
4a – Residual disease
4b – metastatic disease
Carcinoma stomach
 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
 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
 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
 +ve Troisier’s sign
 +ve recto-vesical secondaries (Blumer shelf) on
per rectal examination
 +ve Trousseau sign- migrating thrombophlebitis
(also found in CA-pancreas)
 Gastritis
 Pancreatic mass – carcinoma
 Transverse colon mass – carcinoma
 Acid peptic disease – Pyloric stenosis
Carcinoma stomach
Carcinoma stomach
 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
 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
 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
Carcinoma stomach
 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
 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
 Growth seen in OG junction or upper part of
stomach.
 Upper radical gastrectomy
 Removal of:
 Spleen
 Both the omentum
 LN
 Later oesophagogastric anstamosis
 When growth is in body or Linitis plastica
 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.
 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.
Carcinoma stomach
 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
 Postoperative radiotherapy with chemotherapy
using 5-FU and leucovorin is the standard
adjuvant therapy.
 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
 To palliate pain
 To palliate vomiting
 When there is bleeding
 Improve appetite
 Partial gastrectomy is the best method
 Palliative partial gastrectomy
 Palliative anterior gastro-jejunostomy with
jejuno-jejunostomy
 Endoscopic stenting or dilatation
 Laser decanalisation
 Palliative chemotherapy – FAM regimen
 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
Carcinoma stomach

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Carcinoma stomach

  • 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
  • 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