Gastroduodenal Pathology

Dr Srikumar
Stomach
Gastritis

Inflammation of stomach wall

Acute gastritis- polymorphs- epithelium

Chronic gastritis-
Lymphocytes & plasma cells in lamina propria
intestinal metaplasia
atrophy of mucosa
H pylori infection
Classification of Chronic Gastritis

Distribution in stomach, associated other

morphological features
1. Autoimmune chronic atrophic gastritis
2. H Pylori chronic gastritis- diffuse antral or
multifocal gastric atrophy
3. Chemical Gastritis (reactive gastritis,
reactive gastropathy)
Autoimmune chronic atrophic gastritis

Site- gastric body with sparing of antrum,

not associated with H pylori

Gastric parietal cells and intrinsic factor
(IF) auto-antibodies

Failure to absorb Vit B12 due to lack of IF-
megaloblastic anaemia

Risk of carcinoma - 10% in 20 years.
 H pylori associated gastritis

Gram negative bacteria.

Rod shaped organism, resides
on surface of epithelial cells &
mucus

Identified by urease test on
stomach bx.

Organism produces a potent
urease which splits urea into
ammonia.

Diffuse antral and Multifocal
chronic atrophic gastritis
Helicobacter pylori:

Most common infection in the world (50% of
worlds population; 80% asymptomatic)

10% of men, 4% women develop PUD *

Positive in 70%-100% of PUD patients.

H.pylori related disorders (Hp is present in):
Chronic gastritis – 90%
Peptic ulcer disease – 95%-100%
Gastric carcinoma – 70%
Gastric lymphoma
Reflux Oesophagitis.
Non ulcer dyspepsia
H. pylori
H. pylori – H & E stain
H. pylori – silver stain
Chemical gastritis/ reactive gastritis

Seen in association with:

- Bile reflux: surgery, direct bile injury
- NSAIDs (eg naproxen, indomethacin,
ibuprofen) (decreased prostaglandins
which protect from acid damage)
Damage to mucosa, minimal inflammation
Elongation and tortuosity of foveolae
Treatment of gastritis

Aim at H pylori eradication - risk of
carcinoma and lymphoma

Intestinal metaplasia and autoimmune
gastritis - increased risk of gastric
carcinoma

Triple therapy for 7 d effective in 90%
cases
- Clarithromycin 500mg bd
- Amoxycillin 1g bd/ metronidazole400 mg
bd
- PPI (eg omeprazole 20mg bd)
Inflammation – acute gastritis
Acute gastritis
Chronic atrophic gastritis
Hypertrophic gastritis
Haemorrhage - gastritis
Peptic Ulcer - mechanism
Ulceration in GI tract.
Basic principle: Gastric acid secretion by
peptic cells; Protection of mucosa by
gastric mucus production
Due to increased gastric acid +/- decreased
mucosal resistance to gastric acid
(produced by gastric peptic cells)
Effect occurs in non-acid secreting mucosa
Classification, site & risk factors

Erosion (mucosa only), Acute (mucosa and

submucosa), Chronic (till muscle coat)
Sites - Stomach (antrum), Duodenum (1st
part), Lower oesophagus, Jejenum,
Meckels diverticulum, Umbilicus
Blood group O; Toxic/ injuries- burns, drugs,
cigarette smoking.
Erosion & Acute Peptic Ulcer - causes

Acute stress
Trauma (stress ulcer)

Severe illness
Long term steroids

Sepsis
Aspirin and NSAID

Burns (Curlings ulcer) injestion,

Post surgical op
Lye* – pretzels, rice

CNS neurological dumpling, noodles
disturbance
Radiotherapy
(Cushings Ulcer)

•*USP 2009
Erosion & Acute PU - features

Wide distribution in stomach, first few cm

of duodenum

Mucosa (erosion) and submucosa (Acute
PU)

Small, often multiple, upto 1-2 cm
diameter

Main symptoms and signs- due to
haemorrhage

Usually heal completely without scarring
Erosion
 Chronic PU Stomach

Chronic Gastric Ulceration (GU), age 50+

>90% are solitary, approx 5% multiple

junction between gastric antrum and body on
lesser curve approx 5cm from pylorus,

Morphology- extends through muscle coat,
fibrosis - stomach/ duodenal wall distorted

Round, oval or linear ulcer, converging
mucosal folds, fibrous tissue base
Gastric ulcer
Chronic PU Microscopic features

Similar for GU, DU other sites

Floor- covered with pus.

Base- fibrosis extending till muscle wall

Adjacent mucosa, vessels – inflamed
(granulation)

Fibrosis- adhesions to pancreas,
omentum, liver +/- local perforation
Chronic Duodenal Ulcer (DU)

M>> F , blood group O

Usually single , rarely multiple.

Associated with gastric acid hypersecretion +/-
decreased mucosal resistance

Within first 2 cm of duodenum- less commonly
2nd part duodenum

Punched out ulcer, fibrosis- distortion of
duodenum

Complications - Healing & scarring, Perforation,
Haemorrhage, ? carcinoma
Duodenal ulcer
Giant gastric ulcer
Chronic ulcers Diagnosis & Rx
- Radiology- ulcer seen on barium meal
- Endoscopy- visualise, photograph and
biopsy

Medical Rx – antacids, H2 blockers, >
80% heal in 1 month medical treatment

Remove cause- chronic NSAIDs

Indications for surgery - failure of medical
Tx, complications, recurrence, Giant ulcer
Stomach tumours
Benign Tumours Malignant Tumours

Adenomas
Adenocarcinoma

Leiomyoma
Lymphoma

Endocrine Tumours -
carcinoids

GI Stromal Tumours

Leiomyosarcoma

Kaposi’s Sarcoma
 Gastric Cancer

2nd most common High Low
tumour
E Asia (Korea, SE Asia

1,100,000 affected in China, Taiwan, Japan)
2008-09 (850,000 S America (Chile, N America
deaths) Venezuela)

Diet, Bile reflux, H E Europe rest of
Pylori, DNA damage Europe
(point mutations in E- Africa
cadherin gene), Blood
group A
 Gastric adenocarcinoma and diet
High risk:
Preserved food (nitrites derived from
nitrates)
High intake of nitrate Smoked/cured
meat/fish
High intake of complex
carbohydrates chiefly derived from
grains and tuberous roots
High intake of salt/ Pickled
vegetables/ Chilli peppers
Low intake of protein, green, leafy
vegetables and fruits
Gastric Adenocarcinoma and diet

Benefits of fruit and

vegetables –
anti-oxidant effect
Key protective agents-
Ascorbic acid, alpha
tocopherol,
carotenoids, folate,
Role unclear- alcohol,
tobacco
Helicobacter pylori

Causes : Results of these:

Chronic Intestinal metaplasia
gastritis………… Increased pH-
Decreased acid nitrosated products
secretion………. (carcinogens)
Loss of anti-oxidant
Decreased intra gastric
ascorbic acid DNA point mutations
Increased oxidants……
Definitions for Gastric cancers

Intraepithelial neoplasia = confined to

surface epithelium (dysplasia)
Intramucosal carcinoma = invasion of lamina
propria
Early Gastric Cancer = carcinoma confined
to mucosa or into submucosa
Advanced Gastric cancer = invasion deeper
than submucosa
Gastric Adenocarcinoma
Symptoms and Signs
Often very late in presentation
Persistent abdominal pain, unrelieved by
eating, bleeding (ulceration),
haematemesis, gastric outlet obstruction,
anorexia & weight loss (disseminated
disease)
Diagnosis- endoscopy, multiple punch biopsy,
barium meal, MRI for staging.
Morphology

Localization of tumour Prevalence

Pylorus and antrum
50 to 60%

Cardia
25%

Other areas
15 to 25%
Lesser curvature
40%
Greater curvature
12%
Body : Ant/ post walls
48%
Gastric Adenocarcinoma
macroscopic appearance
Commonest site- distal stomach (antro-
pyloric region, followed by body of
stomach- greater or lesser curve
Advanced Gastric Cancer- polypoid,
fungating, ulcerative, infiltrative
Linitis plastica- diffusely infiltrative ‘leather
bottle stomach’ contracted
Gastric adenocarcinoma
Microscopic classification
WHO classification Lauren classification

Tubular adenoca

Papillary adenoca
Intestinal ca

Mucinous ca
Diffuse infiltrative ca

Signet ring cell adenoca

Undifferentiated

Adenosquamous
 Diffuse type

More frequent in younger
age groups, little difference
between sexes.

Arise from gastric mucosal
cells, not associated with
chronic gastritis.

No glandular pattern seen.
‘Signet –ring’ cells or small
clusters in ‘infiltrative’
pattern.
Intestinal type

More frequent in males
and at older age
groups.

Arise from gastric
mucosal cells that have
undergone intestinal
metaplasia (due to chr
gastritis).

Better differentiated,
resemble colonic
adenocarcinoma.

<<<<Diffuse

Intestinal >>>
EGC
Adenco ca of intestinal type
Linitis plastica
Spread

Direct spread
Transcoelomic dissemination into peritoneal cavity.
Spread into oesophagus/ pancreas/ liver/ common bile
duct/ diaphragm/ spleen and transverse colon.
Krukenberg tumour : Secondary deposits in both ovaries-
from stomach (& breast, pancreas, GB)

Lymphatic spread
Regional lymph nodes (lesser/ greater curvature)
Involvement of the supraclavicular lymph node
(Virchow’s sign ) in some cases.

Haematogenous spread
To liver ,lungs, brain, bones, kidneys /adrenals.
Complications

Haemorrhage : haematemesis +/- melaena.

Obstruction: especially in the pyloric antrum.

Perforation: due to necrosis and penetration
through all the layers.

Jaundice: when there is extension into the
common bile duct / porta hepatis

Ascitis : Fluid accumulation in the peritoneum
Staging and prognosis

TNM staging. Required for both treatment, follow up and
predicting prognosis.

TX = primary tumour (T) cannot be assessed

T0 = no evidence of primary tumour

Tis = carcinoma in situ, no lamina propria invasion

T1 = tumour invades lamina propria or submucosa

T2 = tumour invades muscularis propria/subserosa

T3 = tumour penetrates serosa without invasion of
adjacent structures

T4 = tumour invades adjacent structures .
Gastric Carcinoma Prognosis

Early Gastric Cancer- small mucosal lesions <

4cm - 10 year survival up to 90%
Advanced Gastric cancer- Lymphatic and
vascular invasion- poor prognosis. 5 year
survival 10-44%
Diffuse carcinoma poorer prognosis than
intestinal type
Prognosis worse in younger patients.
Management

Surgical removal of the stomach is the

only curative treatment.

Radiation therapy and chemotherapy
given after surgery improve the chance
of a cure.

For patients in whom surgery is not an
option, chemotherapy or radiation can
improve symptoms.
GIST
NHL: high/ low grade(MALT).
Summary :
Today’s Student learning outcomes

Gastritis - types

Peptic ulcers – Types, clinical features,
complications

Gastric cancers – risk factors

Adenocarcinoma – intestinal, diffuse

Staging, prognosis and management

Investigations – endoscopy, biopsy