description of gastric cancer and duodenal ulcers

1. Carcinoma Stomach
&
Duodenal Ulcer
UF BATCH – 2017
Date- 06/09/2021
Dr. Ankita Singh
Assistant Professor
Department of Surgery

2. How to identify stomach?

3. Normal gross anatomy
• Appearance:
• Volume: 1.5-3L
• Mucosa: fine mosaic like
(punctuations- pits/foveolae)
• Rugae: longitudinal infoldings
– Coarser proximally & empty stomach
• Divided into:
– Cardia, Fundus, Body, Antrum, Pylorus

5. CARCINOMA STOMACH

8. Epidemiology
• 5th most common neoplasm & 3rd most deadly
cancer (GLOBOCAN 2018 data)
• High incidence Japan & better outcome
• India: Southern states more affected
• Environmental disease
• Men more often affected
• Incidence increases with age

9. Epidemiology..
• Distal gastric cancers:
– more common; decreasing trend
– low socioeconomic status
– elderly
– associated with H. pylori, diet, environmental
– Intestinal type
– better prognosis
– 30% resectability
– Distal subtotal gastrectomy

10. Epidemiology..
• Proximal gastric cancers:
– rising trend
– upper socioeconomic status
– young
– Not diet, environmental related
– Diffuse type
– Poor prognosis
– <20% resectable
– Total gastrectomy + reconstruction

11. Aetiology
Familial (10%)
- e cadherin mutation (90%)
- Hereditary diffuse type
Dietary factors
- Red meat, smoked salmon, high salt,
cabbage, preserved food ( nitrosamines),
lead, less vegetables, low vit A & C
- Alcohol intake
- High calorie intake: obesity
Other genetic mutations
- p53 inactivation
- bcl-2 mutation: intestinal type
- Growth factor over expression
- APC gene: intestinal type
- H ras oncogene
- C erb B2 gene
Precancerous conditions
- H. Pylori infection, chronic gastritis
- Gastric dysplasia, intestinal metaplasia
- Benign gastric ulcer
- Pernicious anemia
- Adenomatous polyps >2cm
- Agammaglobulinemia
- Menetrier’s disease
- Previous gastric surgery
Genetic syndromes
- HNPCC, FAP, Li Fraumen Syndrome
Blood group A
Exposure to Zn, Pb, talc, asbestos
First degree relatives of stomach cancer
patient
Monozygotic twins , EBV, radiation ,
occupational (rubber, coal) & smoking

12. Pathology
• Gross types:
– Cauliflower, Ulcerative, Leather-bottle type
• Lauren’s classification (patho-histological):
– Intestinal, Diffuse, Others- Unclassified
• Based on depth:
– Early gastric cancer: T1 + any N
• Japanese classification:
– type I-Protruded, type II- Superficial (a-elevated, b-flat, c-
depressed, type III-Excavated

14. Pathology
• Gross types:
– Cauliflower, Ulcerative, Leather-bottle type
• Lauren’s classification (patho-histological):
– Intestinal, Diffuse, Others- Unclassified
• Based on depth:
– Early gastric cancer: T1 + any N
• Japanese classification
• Mostly well differentiated, high cure rate
• EMR- endoscopic mucosal resection is possible

15. Pathology..
• Based on depth:
– Advanced gastric cancer: >=T2 + any N
• Borrmann's classification:
– I. Single, polypoid carcinoma.
– II. Ulcerated carcinoma with clear cut margin.
– Ill. Ulcerated carcinoma without clear cut margin.
– IV. Diffuse carcinoma- linitis plastica.
– V. Unclassified.

17. Pathology..
• WHO histologic classification:
– Adenocarcinoma-most common
• Papillary adenocarcinoma-most common type
• Tubular adenocarcinoma
• Mucinous adenocarcinoma
• Signet-ring carcinoma
– Adenosquamous carcinoma
– Squamous cell carcinoma-rare, when occurs it is
common near OG junction
– Undifferentiated carcinoma
– Others- unclassified carcinoma

18. Pathology..
• Proximal gastric adenocarcinoma:
– Siewert classification:
•

19. Sites

20. Spread
• Direct:
– Horizontally- submucosal
– Vertically- adjacent organs
• Lymphatic:
– Permeation & embolization of cancer cells
through lymphatics to-
• subpyloric, gastric, pancreaticoduodenal, splenic,
coeliac, aortic, and later to left supraclavicular lymph
nodes
• Retrograde involvement- mesentric nodes of small &
large bowel

21. Spread..
• Lymphatic:
– 4 Zones of lymphatic drainage of stomach
– 4 Lymph node groups: 16 stations/ echelon
– *4 Levels of lymph node dissection: D1-D4

24. Virchow node

25. Spread..
• Hematogenous:
– Liver (common), lung & bones
• Transperitoneal :
– Peritoneal deposits
– Ascites
– Krukenberg’s tumour ovary-
• Retrograde lymphatic spread/ transcelomic spread
– Blumer shelf
– Sister Mary Joseph nodule

26. Clinical presentation
• Asymptomatic :
– early gastric cancer/ cancer of body
• Nonspecific symptoms:
– indigestion/vague epigastric discomfort, constant
nonradiating pain not related to food intake.
• Specific symptoms:
– depend on the site of tumour-obstruction,
dysphagia, mass, etc.

27. Clinical presentation..
• Metastatic disease:
– liver secondaries, ascites, secondaries in ovary,
rectovesical pouch, umbilicus, supraclavicular
nodes, lung and bone secondaries.
• Unusual presentations:
– acanthosis nigricans, Irish node in the left anterior
axillary region.

28. Sign & Symptoms
• Recent onset loss of appetite & weight, early
satiety, fatigue
• Anemia: microcytic hypochromic
• Upper abdominal pain/ discomfort
• Vomiting many hours after meals, containing
undigested food: GOO
– Visible gastric peristalsis, succusion splash +,
auscultopercusion

29. Sign & Symptoms..
• Mass per abdomen
• Dyphagia with mass epigastrium
• Jaundice- unconjugated, palpable nodular
liver, or conjugated hyperbilirubenemia
• Ascites
• Troisier’s sign
• Sister Mary Joseph nodule
• Per rectal: Blumer shelf
• Trousseu sign

30. Sign & Symptoms..
• Haematemesis, malena
• Perforation peritonitis
• Cutaneous nodules
• Krukenberg tumour

31. Investigations
• To confirm the diagnosis:
– Endoscopic biopsy
– Barium study- single/double barium meal
• Irregular filling defect
• Loss of rugosities
• Delayed emptying
• Dilatation of stomach in carcinoma pylorus
• Decreased stomach capacity in linitis plastica
• Margin of the lesion projects outward from the
ulcer/lesion into the gastric lumen-Carmanns meniscus
sign

32. Investigations
• For staging:
– CECT chest, abdomen & pelvis
• TNM , thus operability
– Endoscopic ultrasound & USG abdomen- not ised
for staging
– FNAC palpable left supraclavicular LN
– Staging Laparoscopy
• Supportive tests:
– LFT, PT, Tumour markers (CA 72-4, 19-9,12-5, CEA)
– CBC with peripheral smear

33. Treatment
• Curative resection undertaken if there is
– absence of serosal, peritoneal, hepatic spread;
with free adequate resection margin, with
adequate nodal clearance
• LN dissection (D): exceeds one level more than the N
involvement
• Extended resection: total gastrectomy with distal
pancreatectomy with splenectomy

34. Treatment..
• Early growth in pylorus:
– Subtotal gastrectomy + reconstruction
• Growth OGJ/upper stomach:
– Upper radical gastrectomy/ total radical
gastrectomy + reconstruction
• Growth in body/antrum:
– Subtotal gastrectomy + reconstruction
• Linitus plastica:
– Total radical gastrectomy +reconstruction

36. Treatment..
• D1 dissection
– done for N0
– Group I: stations 3-6 nodes removed (along the lesser and
greater curves and pylorus)
• D2 dissection
– Done for N1
– Group I & II: station 1-11 nodes removed (left gastric/
common hepatic/splenic/retropancreatic)
– Splenic nodes can be cleared with or without splenectomy
along with removal of tail of pancreas.

37. Treatment..
• D3 dissection
– Done for N2
– Group I,II & III: station 1-16 removed (hepatoduodenal,
nodes along mesentery, middle colic)
• D4 dissection
– not commonly advocated
– It is removal of stations 1- 18.

38. Treatment..
• D2 is always better than D1
• At least 15 lymph nodes should be
removed.
D2 gastrectomy and adjuvant chemoradiation is ideal present
concept therapy in operable carcinoma stomach.
Omentectomy (both greater and lesser) and bursectomy
(removal of outer leaf of transverse mesocolon baring colic
vessels) should be added.

39. Treatment..
• Endoscopic mucosal resection
– Early gastric carcinoma
• Protruded
• Ulcer free depressed
– <2cm, elevated, well differentiated, N0
– Technique
• Photodyanamic therapy
– Hematoporphyrin derivative i.v. , 2 days later laser
light to tumour, damage by singlet O2

40. Treatment..
• Neoadjuvant therapy
– Chemotherapy/ chemoradiation
• ECF- Epirubicin, Cisplatin, 5FU
• EAP- Epirubicin, Adriamycin, Cisplatin,
• FDT- FU, Doxorubicin, Triazinate
– Downstage the tumour

41. Treatment..
• Adjuvant therapy
– Chemotherapy
• FAM regime- 5 FU,adriamycin, Mitomycin C
– Chemoradiotherapy
• RT, 5FU, Leucovorin
• Better than CT alone
– Bevacizumab : anti VEGF
– Mitomycin C impregnated charcoal:
• instill intraperitoneally to control lymphatic disease

42. Treatment..
• Adjuvant therapy..
– Intraperitoneal chemotherapy (IPC)
• Can be combined with hypothermia (HIPC)
• Early post operative (EPIC)
• Oxaliplatin
– Transtuzumab:
• moleculat targeted therapy- monoclonal antibody
against HER 2
– Immunochemotherapy
• Principle-improve/modulate T cell- Picibanil + mitom

43. Treatment..
• Palliative therapy
– Inoperable tumour
• Adherent to pancreas or colon or mesocolon
• Ascites
• Para-aortic lymph nodes
• Secondaries in liver
• Palpable mass is incurable but can be resectable
surgically
• Blumer shelf
• Left supraclavicular nodes
• Sister Mary Joseph nodule
• Irish node

44. Treatment..
• Palliative therapy..
– For pain, vomiting, bleeding, decreased appetite
– partial/total gastrectomyis the best palliation
whenever possible- for obstruction, bleeding,
decresing tumour load
• With anterior GJ with J-J anastamosis
– Or bypass surgery: Devine’s exclusion
– Palliative CT
– RT & analgesics
– Endoscopic stents, Mousseau Barbin tubes,
Celestine tubes

45. DUODENAL ULCER

48. Introduction
• Erosions due to disruption of mucosal barrier
• Most commonly involve first part of
duodenum
• Incidence has been falling:
– Widespread use gastric antisecretory agents
– H. pylori eradication therapy
• Peak incidence older age groups
• Common in males

49. Aetiology
• Blood group O+ve
• Stress, anxiety- ‘hurry, worry, curry'
• Helicobacter pylori infection (90%)
• Drugs:
– NSAIDs, Steroids
• Endocrine causes:
– Zollinger-Ellison syndrome, MEN syndrome,
hyperparathyroidism

50. Aetiology..
• Other causes:
– Alcohol, smoking, vitamin deficiency, post
surgeries
• Cushing ulcers
• Dragstedt dictum: "No acid - No ulcer"

51. Pathology
• First part of duodenum (usually with in the
first inch)
– In the bulb (bulbar)-95%;
– Post-bulbar (5%).
• Involves muscular layer
• Can present acute ulcer- Stress, Steroid,
Surgery & NSAIDS

52. Pathology
• Eventually it shows cicatrisation causing
pyloric stenosis
– serosa overlying the site shows petechial
haemorrhages (cayenne pepper)
• Microscopically
– ulcer with chronic inflammation, granulation
tissue, gastric metaplasia of duodenal mucosa,
endarteritis obliterans
• Sometimes kissing ulcers
– anterior ulcer perforates commonly
– posterior ulcer bleeds or penetrates commonly

53. Clinical Features
• Duodenal ulcer (DU) to gastric ulcer is 30: 1
• All socioeconomic group
• More with stressed professionals (type A
personality)
• Pain epigastrium
– May radiate to back
– Intermittent
– More empty stomach : hunger pain
– Early morning & night
– Decreases after taking food

54. Clinical Features..
• Common in males
• Periodicity is more common
• Water-brash, heart burn, vomiting
• Bleeding:
– Chronic- microcytic anemia
– Acute- melaena is more common, haematemesis
also can occur
• Appetite is good and there is gain in weight. It
decreases once stenosis develops

55. Sequalae
• Pyloric stenosis (10%)
• Bleeding (10% )
• Perforation (5%)
– Both acute and chronic ulcers
– Anterior ulcers
• Residual abscess
• Penetration to pancreas
• Giant duodenal ulcer

59. Sequalae..
• Intractability:
– Ulcer not healed after 8 weeks of anti-ulcer drugs
• Recurrence:
– Healed once, only to recur again
• Chronic duodenal ulcers generally do not turn
malignant

60. Investigations
• Barium meal:
– Deformed/ absent duodenal cap
– Trifoliate duodenum
• UGI Endoscopy:
– Type, location, complication
– Biopsy
• S. Gastrin levels

63. Treatment
• Aim- relieve symptoms, heal ulcer, prevent
complications & recurrence
• General measures:
– Avoid drugs- NSAIDs, Steroids; alcohol, smoking,
spicy food
– Take frequent meals
• Drugs
• Surgery

64. Treatment..
• Drugs
– H2 Blockers
• Reduce acid secretion- promote healing in 4-8wks
• Cimetidine, Ranitidine, Famotidine etc.
– PPI- Proton Pump Inhibitors
• Inhibit H+- K+ ATPase enzyme
• Stop acid secretion
• Takes 6-12 wks
• Omeprazole, Lanzoprazole, Pantoprazole, Esmoprazole,
etc.

65. Treatment..
• Drugs
– Antacids
• Neutratise HCl & inhibit peptic activity
• Al(OH)3 & Mg2O8Si3
– Sucralfate
• binds to ulcer bed and stays for 12 hours ; prevents
back diffusion of hydrogen ion; raises endogenous
prostaglandin level in tissues; binds bile acid and
pepsin; prevents colonisation of gastric mucosa by
bacteria.
• protective coat to ulcer crater thereby promotes
healing
• Aluminium salt of sulfated sucrose

66. Treatment..
• Drugs
– Anti-Helicobacter pylori regime:
• given for 7-14 days-later the protonpump inhibitors are
continued
• Triple or quadruplet regimes
• Colloid bismuth sulphate is a good drug for ulcer, but
stains
– Misoprostol:
• increase mucus and bicarbonate secretion, improves
mucosal blood flow, reduces acid secretion.
• only prostaglandin agonist accepted
• PG E1 (mesoprostol) and E2

67. Treatment..
• Surgery
– Indications:
• Uncomplicated duodenal ulcer : HSV (highly selective
vagotomy)
– Intractable
– Recurrent
• Complicated
– Pyloric stenosis : HSV + GJ
– Bleeding with hemodynamic instability : endoscopic
cauterization/clipping/ sclerotherapy, DSA + embolisation,
underrunning of bleeder, ligation of GDA
– Perforation : Celan Jones, Graham’s patch, modified Graham’s
patch

75. Thank you