8. Stomach
Functions
◦ Mix food
◦ Reservoir
◦ Start digestion of
Protein
Nucleic acids
Fats
◦ Activates some enzymes
◦ Destroy some bacteria
◦ Makes intrinsic factor –
B 12 absorption
◦ Destroys some bacteria
◦ Absorbs
Alcohol
Water
Lipophilic acid
B 12
8
9. Bezoar
A bezoar is a mass found trapped in
the gastrointestinal system (usually
the stomach), though it can occur in
other locations.
A pseudobezoar is an indigestible
object introduced intentionally into the
digestive system.
There are several varieties of bezoar,
some of which have inorganic
constituents and others organic.
11. Pyloric stenosis
In 95% of infants with pyloric stenosis
the age at presentation is between 3
and 12 weeks of life, typically between
3 and 8 weeks.
Pyloric stenosis has been reported in
neonates within the first day of life.
11
13. etiology
3 in 1,000 live births
more commonly in males
30 percent of cases occur in firstborn
genetic predisposition
Sibling has 5 times more incidence
environmental factors
Neonatal hypergastrinemia and gastric
hyperacidity may have a role
13
14. CLINICAL MANIFESTATIONS
The classic presentation of IHPS
is the three- to six-week-old baby
who develops immediate
postprandial, non-bilious, often
projectile VOMITING and
demands to be re-fed soon
afterwards
(a "hungry vomiter").
14
15. Palpable mass
The mass is most easily felt
immediately after emesis because it
may otherwise be obscured by a
distended antrum and/or tensed
abdominal muscles
15
16. Pancreatic heterotopia
Pancreatic tissue outside boundaries
of pancreas without anatomic or
vascular connections to pancreas
● Also called ectopic pancreas
● Present in 0.5% to 14% of autopsies
● Due to displacement of pancreatic
tissue during embryonic development
16
21. Pathophysiology
The mechanisms of mucosal injury in gastritis is thought
to be an imbalance of
aggressive factors
acid production or pepsin
and
defensive factors
mucus production
bicarbonate
and blood flow
21
24. Classification of gastritis
Acute Chronic
•H pylori gastritis
•Other infective gastritis – bacteria,
virus, fungi, parasite
•Acute non infective gastritis
•Type A- autoimmune
•Type B- h pylori related
•Type AB- environmental
•Chemical – reflux gastritis
•Uncommon forms
24
25. Acute & Chronic Difference
◦ Acute refers to short term inflammation
◦ Acute refering to neurophilic infiltrate
◦ Chronic referring to long standing forms
◦ Chronic referring to mononuclear cell
infiltrate especially lymphocyte and
macrophages
25
26. Acute Gastritis
Definition
◦ An acute mucosal inflammatory
process, with neutrophilic infiltrate,
that is usually transient.
◦ There may be hemorrhage into the
mucosa or sloughing of the mucosa.
◦ Severe erosive form is an important
cause of severe GI bleeding
26
27. Etiology
◦ Frequently associated with, among others:
heavy use of NSAIDS, especially aspirin
excessive alcohol consumption
heavy smoking
severe stress e.g. trauma, burns, surgery
Ischemia
Systemic infection
◦ Often, idiopathic
27
28. NSAIDs
NSAIDs and aspirin also
interfere with the protective
mucus layer by inhibiting
mucosal cyclooxygenase
activity, reducing levels of
mucosal prostaglandins
28
29. Smoking
Promotes gastritis & ulcer occurrence
Increases the likelihood of
ulcer complications
Mechanisms
◦ Stimulate gastric acid secretion
◦ Stimulate bile salt reflux
◦ Causes alteration in mucosal blood flow
◦ Decrease mucus secretion
◦ Reduces prostaglandin synthesis
◦ Decrease pancreatic bicarbonate secretion
29
30. Acute Gastritis - Pathogenesis
30
All above Factor Acid secretion
+ back diffusion
+ Bicarbonate
buffer
+
Blood flow
Disruption
of
Mucus layer
+
Direct
Mucosal
Injury
Acute Gastritis
31. Stages of Acute Gastritis
Acute superficial
gastritis
Inflammation of
superficial
gastric mucosa.
Acute erosive
gastritis
Destruction of
multiple small
zones of superficial
mucosa.
Acute Gastric Ulceration
Destruction of full thickness of mucosa
31
33. Acute Gastritis - Morphology
Ranges from edema with neutrophil infiltration, vascular congestion,&
an intact epithelium, to erosion (mucosal defect that does not cross
the muscularis mucosa) and hemorrhage.
33
38. Chronic Gastritis
Definition
◦ Chronic mucosal inflammatory changes
leading to atrophy and metaplasia
(usually without erosions)
Dysplasia and ultimate neoplasia are
complications.
38
46. Pathogenetic qualities of H.pylori;
Adheres to gastric epithelium
Lives within mucous gel layer overlying gastric epithelium
Penetrates intercellular junctions
Invades gastric glands and canaliculi of parietal cells
Secretes urease to produce ammonia, which protects it from
gastric acid
Produces cytotoxins that may play role in pathogenicity
Induces epithelial cytolysis and disrupts intercellular
junctions
Increases permeability of mucous layer to hydrogen ions
and pepsin
Enables gastric acid and pepsin to create ulcer craters
Evades host immune defenses
Damages tissue.
46
50. Helicobacter gastritis
2 patterns of infection
◦ Diffuse involvement of body and antrum
(“pan gastritis” associated with
diminishing acid output)
◦ Infection confined to antrum (antral
gastritis, associate with increased acid
output)
50
51. Type A (Auto immune)
Etiology
◦ Autoimmune - antibodies to parietal cells,
gastrin receptor, intrinsic factor, and H+,K+
ATPase
<10% of cases of chronic gastritis
Possible autosomal dominant inheritance
51
52. Morphology of chronic gastritis
Chronic inflammatory cell
infiltration
Mucosal atrophy
Intestinal (goblet cell)
metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
52
53. Autoimmune gastritis
Autoimmune gastritis -
pernicious anemia
Chronic atrophic
gastritis is associated
with Ab’s
- intrinsic factor
- patietal cell
bright green IF- in the
parietal cells of the
gastric mucosa.
53
55. Chronic Gastritis
Clinical Features
◦ Usually only a few symptoms: nausea,
vomiting, upper abdominal discomfort
◦ Autoimmune
Hypo to achlorhydria (severe loss of
parietal glands)
Hypergastrinemia
10% have pernicious anemia
55
56. Clinical Complications
◦ Autoimmune:
Often seen in association with other
autoimmune disorders (Hashimoto
thyroiditis, Addison disease, and type I
diabetes)
Significant risk for the development of
gastric carcinoma (2-4%) and
endocrine tumors (carcinoid tumor)
56
57. Chronic Gastritis
Morphology
◦ Varying degrees of mucosal damage
possible
◦ Mucosal lesions are reddened, with
thickened rugae
◦ Atrophied rugae in long-standing cases
◦ Lymphocytes and plasma cell infiltrate;
neutrophils indicate “active” inflammation
(may or may not be present)
57
58. ◦ Regeneration - constant feature
◦ Metaplasia - mucosa of antral and
body-fundic regions converts to
columnar absorptive cells and goblet
cells (intestinal metaplasia)
◦ Atrophy - marked loss of glands
◦ Dysplasia – precursor lesion to gastric
cancer in atrophic gastritis
58
59. Sydney System of
Grading Chronic Gastritis
1. Site: Antral, Corporal mucosa
2. Grading of: (Mild, Moderate, Marked)
H-Pylori
Chronic inflammation
Activity
Atrophy
Intestinal metaplasia
*Normal lymphocytes & plasma cells in lamina propria = up to
5/HPF
*No Neutrophils in lamina propria
61. Peptic Ulcer Disease
Condition characterized by
◦ Erosion of GI mucosa resulting from
digestive action of HCl and pepsin
62. Peptic Ulcer Disease
Ulcer development
◦ Lower esophagus
◦ Stomach
◦ Duodenum
◦ 10% of men, 4% of women
63. Types
Acute
◦ Superficial erosion
◦ Minimal erosion
Chronic
◦ Muscular wall erosion with formation of
fibrous tissue
◦ Present continuously for many months or
intermittently
64. Peptic Ulcer Disease
Etiology and Pathophysiology
Develop only in presence of acid
environment
Excess of gastric acid not necessary
for ulcer development
Person with a gastric ulcer has normal
to less than normal gastric acidity
compared with person with a duodenal
ulcer
65. Peptic Ulcer
Size – variable; 0.3 – 4 cm in
diameter
Shape - round to oval
Sharply demarcated, clean-cut,
punched-out area with clean base
Margins are usually level with
surrounding mucosa or slightly
elevated due to edema; the mucosa
is undermined at the edges
Radiating mucosal rugae
80% are solitary, 80% occur in the
duodenum, of which 90% in the
first part of the duodenum on the
anterior wall’ within a few
centimeter of the pyloric ring.
19% occur in the stomach(usually at
the lesser curvature at the border of
the body and antrum.
65
71. Microscopy:
Overhanging gastric
mucosal margins (A)
Necrotic fibrinoid
debris (B)
Acute inflammatory
infiltrate (C)
Granulation tissue
(D)
Fibrotic scarred
base (E)
71
A
B
C, D
E
72. Ulcer Base
Superficial thin layer of
necrotic fibrinoid debris
Zone of inflammatory
infiltrate with neutrophils
Zone of granulation
tissue with dilated blood
vessels and lymphocytes
Zone of fibrous scarring
72
74. Gastric ulcerDuodenal Ulcer
middle age 50-60Any age specially 30-40Age
More in maleMore in maleSex
SameStress job eg. ManagerOccupation
Epi. Can radiate to
back
Epigastric , discomfortPain
Immediately after
eating
2-3 hours after eating &
midnight
Onset
EatingHungerAgg.by
75. Gastric ulcerDuodenal Ulcer
Lying down or vomitingEatingRelived by
Few weeks1-2 monthsDuration
Common(to relieve the
pain)
UncommonVomiting
Pt. afraid to eatGoodAppetite
Avoid fried foodGood , eat to relieve the painDiet
wt. LossNo wt. lossWeight
60%40%Hematemesis
40%60%Melena
76. GASTRIC TUMORS
BENIGN:
POLYPS (HYPERPLASTIC vs. ADENOMATOUS)
LEIOMYOMAS (Same gross and micro as sm. muscle)
LIPOMAS (Same gross and micro as adipose tissue)
MALIGNANT
(ADENO)Carcinoma
LYMPHOMA
POTENTIALLY MALIGNANT
G.I.S.T. (Gastro-Intestinal “Stromal” Tumor)
CARCINOID (NEUROENDOCRINE)
79. GC is not far from us……
Napoleon‘s gastric cancer:tumor
found on the lesser curvature of
the stomach: What cause? How
to treat?
Ambition is never content, even on the
summit of greatness.
He conquered the larger part of Europe,
but he could not conquer gastric cancer
80. How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
81. How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
82. GC Worldwide incidence
Male 16.4
Female 8.2
Male 36.3
Female 16.9
Male 77.9
Female 33.3
Male 10.8
Female 4.9
Male 43.6
Female 19.0
Male 5.9
Female 2.6
Male 11.5
Female 4.3
Male 18.6
Female 13.3
Male 8.4
Female 4.0
Eastern
Europe
Japan
Australia/
New Zealand
China
Northern
Africa
Southern
Africa
Central
America
Western
Europe
North
America
In terms of geographic distribution, high
rates apply to Japan, China and Eastern
Europe and low rates to North America.
Almost 40% of cases occur in China .
Pazdur R et al. Cancer management: A multidisciplinary
approach. edition,2002
85. “The new study suggest he was
chronically infected with the
bacteria Helicobacter pylori.”
“full of salt-preserved foods but
sparse in fruits and vegetables--
common fare for long military”
H. pylori
Genetic factors
“his father had also died of
stomach cancer which led to
the theory that he had
inherited the disease.”
Diet
Precancerous
changes
Why Napoleon died of GC
chronic atrophic gastritis?
86. How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
87. Early gastric cancer
Defined as a tumor confined to the mucosal or submucosal
layer, with or without lymph node metastasis
89. Morphology
SITE - Favoured location is the
lesser curvature of the antropyloric region
Gastric carcinoma is classified on the basis of
- depth of invasion
- macroscopic growth pattern
- histologic subtype
91. Gross: Linitis
plastica carcinoma
diffusely infiltrates
the entire gastric
wall without forming
an intraluminal
mass. The wall of
the stomach is
typically thickened
to about 2-3 cm.
and has a leathery,
inelastic
consistency.
92. Lauren classification
Intestinal type
--- associated with most
environmental risk factors
--- carries a better prognosis
--- shows no familial history
Diffuse type
--- consists of scattered cell
clusters with poor prognosis
93. Intestinal type gland
formation by malignant
cells,
Gastric carcinoma.
Diffuse type demonstrating
signet-ring carcinoma cells.
94. Bormann classifications
Gross classification
phymatoid type
ulcerative type
infiltrative ulcerative
diffuse infiltrative type
96. TNM classification ——T
Primary tumor:
depth of tumor
invasion
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
97. T:Primary tumor
Direct extension into omentum, pancreas,
diaphragm, transverse colon, and
duodenum.
If lesion extends beyond wall to a free
peritoneal surface, peritoneal involvement
is frequent.
98. TNM classification ——N
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
99. TNM classification ——M
Distant metastasis
MX- cannot be assessed
M0- no distant metastases
M1-distant metastases
101. Special term
Blumer shelf
A shelf palpable by reactal examination, due to
metastatic tumor cells gravitating from an abdominal
cancer and growing in the rectovesical or rectouterine
pouch
Krukenberg tumor
A tumor in the ovary by the spread of stomach cancer
102. What is the classification for Napoleon
,
GC
“The scientists suggest that Napoleon died
from a T3N1M0 (stage IIIA)
gastric cancer. This means the tumour (T3)
had spread to some local lymph nodes (N1)
near the stomach, but had not spread or
metastased (M0) to other organs. The
prognosis for such tumours is known to be
very poor. ”
103. How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
104. Clinical manifestation
Early Gastric Cancer
Asymptomatic or silent 80%
Peptic ulcer symptoms 10%
Nausea or vomiting 8%
Anorexia 8%
Early satiety 5%
Abdominal pain 2%
Gastrointestinal blood loss <2%
Weight loss <2%
Dysphagia <1%
105. Clinical manifestation
Advanced Gastric Cancer
Weight loss 60%
Abdominal pain 50%
Nausea or vomiting 30%
Anorexia 30%
Dysphagia 25%
Gastrointestinal blood loss 20%
Early satiety 20%
Peptic ulcer symptoms 20%
Abdominal mass or fullness 5%
Asymptomatic or silent <5%
106. Special signs
Linitis plastica:
--- diffusely infiltrating with a rigid stomach
Virchow’s node:
--- left supraclavicular lymph node
Sister Mary Joseph’s node:
--- umbilical lymph node
prerectal pouch mass (Blumer shelf)
--- seeding metastasis
108. Laboratory tests
Assists in determining optimal therapy.
CBC identifies anemia, with may be caused by bleeding,
liver dysfunction, or poor nutrition.
30% have anemia.
Tumor markers
CEA:carcino-embryonic antigen
CA19-9:carbohydrate antigen
CA724:carbohydrate antigen
109. Imaging Studies
Endoscopic diagnosis
--- biopsy needed for definitive diagnosis
Endoscopic screening
--- general population or high risk persons
110. How to diagnose Napoleon
,
GC
Endoscopic diagnosis?
Endoscopic Ultrasonography?
CT scan? Preoperative staging
......
Why?
111. How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
112. G.I.S.T. TUMORS
Can behave and/or look benign or malignant
Usually look like smooth muscle, i.e., “stroma”
Are usually POSITIVE for
c-KIT (CD117), i.e., express this antigen on immunochemical staining, the tumor cells are derived from the interstitial cells, of Cajal, a “neural”
type of cell
113. G.I.S.T. TUMORS
c-KIT (receptor for stem cell factor)
mutations
platelet-derived growth factor
receptor-a. (PDGFRA) mutations
tyrosine kinase inhibitor (STIS71) has
been shown to be effective in
treatment
115. CARCINOID TUMOR
arise from the diffuse components of the
endocrine system
majority are found in the GI tract, and more
than 40% occur in the small intestine
tracheobronchial tree and lungs
116. Gastric carcinoids
release peptide and nonpeptide
hormones to coordinate gut function
carcinoids are intramural or
submucosal masses that create small
polypoid lesions
120. The most important prognostic factor for GI carcinoid
tumors is location
Foregut carcinoid tumors
rarely metastasize and are generally cured by resection
Midgut carcinoid tumors
Aggressive, greater depth of local invasion, increased size, and presence of
necrosis and mitosis are associated with poor outcome
Hindgut carcinoids occur in appendix & rectum
in appendix almost uniformly benign < 2cm
Rectal carcinoid rarely metastsize
121. GASTRIC LYMPHOMA
Primary :
Mucosa (gut)-associated lymphoid tissue tumor
Previously called
MALToma, MALT-type lymphoma, or MALT lymphoma,
Now called
Extranodal marginal zone B-cell lymphoma of MALT type
lymphoepithelial lesion (LEL) is a hallmark
Secondary
spread from adjacent lymph nodes