Date post: | 15-Jul-2015 |
Category: |
Health & Medicine |
Upload: | drsapna-harsha |
View: | 468 times |
Download: | 2 times |
Dr Sapna M
NORMAL ANATOMY/ HISTOLOGY
Stomach - Normal
3
The normal gastric mucosa
Cardia – mainly mucus-secreting cells
Fundus (body) – acid producing parietal cells, pepsin producing chief cells
Pylorus – hormone (gastrin) production
4
Stomach - Normal
5
6
7
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
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 inorganicconstituents and others organic.
Stomach pathology
Congenital anomaly – pyloric stenosis
Inflammatory conditions – gastritis,
peptic ulcers
Tumors
10
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
12
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
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
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
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
17
Inflammatory
Disease of Stomach
18
Definition
The term gastritis is used to denote inflammation associated with mucosal injury.
.
19
20
PathophysiologyThe 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
Protective factors vs. hostile factors
22
Gastritis
Acute Chronic
23
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
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
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
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
NSAIDs
NSAIDs and aspirin also
interfere with the protective
mucus layer by inhibiting
mucosal cyclooxygenase
activity, reducing levels of
mucosal prostaglandins
28
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
Acute Gastritis - Pathogenesis
30
All above Factor Acid secretion
+ back diffusion+ Bicarbonate
buffer
+
Blood flow
Disruption
of
Mucus layer +
Direct
Mucosal
Injury
Acute Gastritis
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 mucosa31
Mucosal congestion ,edema
inflammation & ulceration
ACUTE GASTRITIS -
MORPHOLOGY
32
Acute Gastritis - MorphologyRanges from edema with neutrophil infiltration, vascular congestion,&
an intact epithelium, to erosion (mucosal defect that does not cross
the muscularis mucosa) and hemorrhage.
33
Acute Gastritis
Gastric mucosa
demonstrates
infiltration by
Neutrophils
34
35
Acute Gastritis
diffusely hyperemic
gastric mucosa
causes for acute
gastritis
◦ alcoholism
◦ drugs
◦ infections, etc.
36
Complications:
Malignancy
Hemorrhage
Perforation
Obstruction
37
Chronic Gastritis
Definition
◦ Chronic mucosal inflammatory changes
leading to atrophy and metaplasia
(usually without erosions)
Dysplasia and ultimate neoplasia are
complications.
38
Chronic Gastritis
Type B
Antral Gastritis
Type A
Autoimmune gastritis
39
40
Type B (Antral Gastritis)
◦ 90% of patients with antral chronic gastritis: Helicobacter pylori infected
Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium.
Pathogenesis◦ H. pylori (urease NH4
+ + toxins) + Host (acid + peptic enzymes) Chronic Inflammation
◦ Antibodies Gland destruction + Mucosal atrophy acid intrinsic factor (which can lead to pernicious anemia)
41
Helicobacter pylori infection
H. pylori – silver stain
43
H. pylori – giemsa stain
44
H. pylori – H & E stain
45
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
47
Noninvasive
Urea Breath Test (UBT) Blood test
Invasive
Biopsy Urease TestHistology
Culture
Stool antigen test
Upper gastrointestinal (upper GI) X-ray
Other tests
Endoscopy
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
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
Morphology of chronic gastritis
Chronic inflammatory cell
infiltration
Mucosal atrophy
Intestinal (goblet cell)
metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
52
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
Autoimmune Gastritis -Morphology
PJ Goldblatt, MD
Diffuse mucosal damage of the body and fundic
mucosa. Antrum less involved.
54
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
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
Chronic GastritisMorphology
◦ 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
◦ 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
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
Peptic Ulcer Disease
Peptic Ulcer Disease
Condition characterized by
◦ Erosion of GI mucosa resulting from
digestive action of HCl and pepsin
Peptic Ulcer Disease
Ulcer development
◦ Lower esophagus
◦ Stomach
◦ Duodenum
◦ 10% of men, 4% of women
Types
Acute
◦ Superficial erosion
◦ Minimal erosion
Chronic
◦ Muscular wall erosion with formation of
fibrous tissue
◦ Present continuously for many months or
intermittently
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
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
Gastric Ulcer- Endoscopic Appearance
66
Gastric Ulcer- Gross Appearance
Sharply punched-out
Large, mucosal defect or ulcer
Radiating mucosal folds
67
Acute Gastric Ulcer
68
Giant gastric ulcer
69
Duodenal Peptic Ulcers- Gross
70
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
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
73
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
Gastric ulcerDuodenal UlcerLying 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. Loss No wt. lossWeight
60%40%Hematemesis
40%60%Melena
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)
WHO GASTRIC NEOPLASMS
Epithelial Tumors:
Adenomatous polyps
Adenocarcinoma (papillary, tubular, mucinous, signet
ring, adenosquamous, unclassified),
Small cell, Carcinoid (neuroendocrine)
Nonepithelial Tumors: Leiomyooma, Leimyosarcoma,
Schwannoma, GIST, Granular Cell Tumor, Kaposi
sarcoma
Malignant Lymphomas:
What is gastric cancer?
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
How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
GC Worldwide incidence
Male 16.4Female 8.2
Male 36.3Female 16.9
Male 77.9Female 33.3
Male 10.8Female 4.9
Male 43.6Female 19.0
Male 5.9Female 2.6
Male 11.5Female 4.3
Male 18.6Female 13.3
Male 8.4Female 4.0
Eastern Europe
Japan
Australia/New Zealand
China
Northern Africa
Southern Africa
Central America
WesternEurope
NorthAmerica
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
Gastric
Cancer
H. pylori
Precancerouschanges
Genetic factors
Diet
Etiological Factors of GC
Precancerous changes
precancerous diseases
chronic atrophic gastritis
gastric ulcer
gastric polyps
gastric remnant
precancerous lesion
atypical hyperplasia
“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
Precancerouschanges
Why Napoleon died of GC
chronic atrophic gastritis?
How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
Early gastric cancer
Defined as a tumor confined to the mucosal or submucosal
layer, with or without lymph node metastasis
Advanced gastric cancer
invasion depth beyond submucosal layer
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
ADENOCARCINOMA
GROWTH PATTERNS
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.
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
Intestinal type gland
formation by malignant
cells,
Gastric carcinoma.
Diffuse type demonstrating
signet-ring carcinoma cells.
Bormann classifications
Gross classification
phymatoid type
ulcerative type
infiltrative ulcerative
diffuse infiltrative type
Histology classification
Adenocarcinoma occupy 95%
Lymphomas 2%
Carcinoids 1%
Adenocathomas 1%
Squamous cell 1%
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
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.
TNM classification ——N
Regional Lymph NodesNX- 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
TNM classification ——M
Distant metastasisMX- cannot be assessed
M0- no distant metastases
M1-distant metastases
Spread Patterns
Direct invasion
Lymph node dissemination
Blood spread
Intraperitoneal colonization
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
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. ”
How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
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%
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%
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
Sister Mary Joseph’s node
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
Imaging Studies
Endoscopic diagnosis
--- biopsy needed for definitive diagnosis
Endoscopic screening--- general population or high risk persons
How to diagnose Napoleon,GC
Endoscopic diagnosis?
Endoscopic Ultrasonography?
CT scan? Preoperative staging
......
Why?
How to diagnose
What is epidemiology and etilogy
What is the pathology
How to treat
Content
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
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
GIST
114
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
Gastric carcinoids
release peptide and nonpeptide
hormones to coordinate gut function
carcinoids are intramural or
submucosal masses that create small
polypoid lesions
Carcinoid tumor
117
119
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
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
Peptic ulcers
Gastric carcinoma
122
123