Lec 2 The stomach pdf - حيدر عبد الرضا

Stomach Pathology

Gastritis

• Acute

– Causes: infectious, chemical
– Histologically: Edema, hyperemia, mucosal erosions and

hemorrhage.

• Chronic

– Helicobacter pylori infection (type B, antral, chronic active

with lymphoid follicles)

– Autoimmune (type A, body, atrophy, pernicious anemia)
– Chemical (induced by drugs, bile reflux, alcohol(

Nonspecific symptoms, abdominal pain

The pathogenesis of acute ulceration

• NSAID-induced ulcers are caused by direct chemical

irritation as well as cyclooxygenase inhibition, which
prevents prostaglandin synthesis.

This eliminates the protective effects of prostaglandins,

which include enhanced bicarbonate secretion and
increased vascular perfusion.

• Lesions associated with intracranial injury are thought

to be caused by direct stimulation of vagal nuclei, which
causes gastric acid hypersecretion.

•Systemic acidosis, a frequent finding in critically

ill patients, also may contribute to mucosal
injury by lowering the intracellular pH of
mucosal cells.

•Hypoxia and reduced blood flow caused by

stress-induced splanchnic vasoconstriction also
contribute to acute ulcer pathogenesis.

Acute gastric ulcers

Macroscopic finding

It range in depth from shallow erosions caused by superficial

epithelial damage to deeper lesions that penetrate the

mucosa.

Acute ulcers are rounded and typically are less than 1 cm in

diameter.

The ulcer base frequently is stained brown to black by acid

digested extravasated red cells, in some cases associated

with transmural inflammation and local serositis. While these

lesions may occur singly, more often multiple ulcers are

present within the stomach and duodenum.

Acute stress ulcers are sharply demarcated,

with essentially normal adjacent mucosa,

although there may be suffusion of blood into

the mucosa and submucosa and some

inflammatory reaction.

Acute gastritis

Gross view showing punctate erosions in an otherwise

unremarkable mucosa; adherent blood is dark due to exposure to
gastric acid.

Low-power microscopic view of focal mucosal disruption with

hemorrhage; the adjacent mucosa is normal.

Chronic gastritis

• Epithelial damage: increase of nuclei, distorsion of foveolae

and glands)

• Mucosal infiltrates of lymphocytes and plasma cells
• Active process: neutrophil granulocytes (acute damage of

epithelial cell)

• Atrophy: chief and parietal cell loss and replacement by

intestinal type epithelial cells

• Intestinal metaplasia: acid mucin containing goblet cells,

microvilli, Panneth cells

• Regenerative changes: foveolar hyperplasia, increase of

myofibroblasts and capillaries

Chronic gastritis
partial replacement of the gastric mucosal epithelium by intestinal
metaplasia (upper left) and inflammation of the lamina propria
(right) containing lymphocytes and plasma cells.

Helicobacter associated chronic gastritis

• Gross: red mucosa, coarser texture than normal,

may have thickened rugal folds or thin/flat

mucosa; with long term disease, mucosa may be

thin/flat; usually affects antrum (particularly in

children), and cardia .

Micro:
Bacteria  is  curved,  spirochete-like,  in
superficial mucus layer and along microvilli of
epithelial cells; are (not invasive); are usually
not  seen  in  areas  of  intestinal  metaplasia;
associated

with

chronic

inflammatory

infiltrate  with  germinal  centers  (follicular
gastritis)  and  plasma  cells  in  lamina  propria;
active  inflammation  if  neutrophils  in
glandular or surface epithelial layer

Helicobacter pylori.

Steiner silver stain demonstrates the numerous darkly stained

Helicobacter

organisms along the luminal surface of the gastric

epithelial cells.
Note that there is no tissue invasion by bacteria.

Helicobacterpylori disease associations. The size of the arrow
is a rough indication of the clinical magnitude of the
association. MALToma = mucosal associated lymphoid
tumours

PEPTIC ULCER DISEASE

• Ulcer: focal destruction of mucosa or deeper (necrosis)

• Erosion: less than full thickness focal loss of mucosa, can

progress to ulcer or heal without scarring.

• Peptic : primary autodigestive lesion caused by the action of

gastric juice.

• Sites: Esophagus, stomach, duodenum and ectopic mucosa

Hyperacidity.

Decreased mucosal protection.

Diagram of causes of, and defense mechanisms against,
peptic ulceration.

Diagram of the base of a non perforated peptic ulcer, demonstrating the layers
of necrosis (N), inflammation (I), granulation tissue (G), and scar (S), moving
from the luminal surface at the top to the muscle wall at the bottom.

Complications of ulcer

• Bleeding

• Perforation

• Obstruction

• Penetration

• Pain

Complications of gastric ulcer:
Bleeding
1.

Occurs in 15% to 20 % of patients.

Most frequent complication.

May be life-threatening.

Accounts for 25% of ulcer deaths.

May be the first indication of an ulcer.

Perforation
1.

Occurs in up to 5% of patients.

Accounts for two thirds of ulcer deaths.

It is rarely the first indication of an ulcer.

Obstruction
1.

Mostly in chronic ulcers.

Secondary to edema or scarring.

Occurs in about 2% of patients.

Most often associated with pyloric channel ulcers.

May occur with duodenal ulcers.

Causes incapacitating crampy abdominal pain.

Can rarely cause total obstruction and intractable vomiting.

Predisposing factors for peptic ulcer of

stomach and duodenum

• Helicobacter pyIori

– direct mucosal injury
– increased acid secretion
– inflammatory reaction

• Trauma: surgery, fractures, burns (Curling ulcer)

• Stress.

• Cerebral Lesions.

– Vagus nerve stimulation (hypothalamus)

• Smoking.
• Zollinger-Ellison syndrome.

– gastrin overproduction, tumor (gastrinoma)

• Genetic Factors.
• Steroid hormons and Nonsteroidal anti-inflammatory drugs.

– blocks prostaglandin synthesis.

Peptic ulcer of the duodenum.

Note that the ulcer is small (2 cm) with a sharply
punched-out appearance. Unlike cancerous ulcers, the
margins are not elevated.
The ulcer base is clean.

TUMORS

• Benign Epithelial Tumors:

• Hyperplastic and inflammatory polyps
• True adenomas rare and not the leading cause of carcinoma

• Malignant Epithelial Tumors:

– Adenocarcinoma

• Malignant Non - Epithelial Tumors:

– Lymphoma

• Potentially Malignant Tumors:

– Endocrine tumors (carcinoid)
– GIST

Gastric tumors

• Polyps

Uncommon 0.4% of adults at autopsy as compared

to colon polyps in 25-50% of adults at autopsy.

Many types

Hyperplastic- response to damage.

Fundic gland polyp: small hamartoma.

Note:

(hyperplastic and fundic gland polyps have no malignant

potential)

Adenomatous polyp have malignant potential!

Pedunculated gastric adenoma

Gastric adenoma
Gross photograph showing a large polyp in the stomach.

Etiologic factors of stomach carcinoma

1. Related to socioeconomic level and diet.
2. High incidence in Japan, actually is decreasing in the

Western world, continue to be high in Asia and Russia.

3. Smoked, salted foods.
4. Low fresh vegetable diet.
5. Nitrosamines.
6. Chronic gastritis with atrophy and metaplasia.
7. H. pylori infection.
8. Intestinal reflux.
9. Blood group A.
10. Relatives with stomach cancer.

Precancerous lesions

• Dysplasia

– Enlarged, hyperchromatic, irregularly outlined, crowded

nuclei.

– Irregular glands, mitoses.

High grade dysplasia = in situ carcinoma =

intraepithelial neoplasia.

• Adenoma

Malignant neoplasms of the stomach:

• Gastric Adenocarcinoma (~ 95%).

• Squamous Cell Carcinoma.

• Adenoacanthoma.

• Carcinoid.

• Gastrointestinal stromal tumors.

• Lymphoma.

Carcinoma of the stomach

• Sites: classically prepyloric, antral and lesser curvature.
• Macroscopic types (Borrmann I-IV):
polypoid, ulcerative, ulcerating and infiltrating,

infiltrating.

• Microscopic types (Laurens):

Intestinal:

  Gland forming, distal, better differentiated, usually old.
  Diffuse:
  Proximal, intracellular mucus, signet ring cells, less

differentiated, usually young patient.

Lauren classification System for gastric adenocarcinoma

Intestinal

•  Environmental.
•  Gastric atrophy with intestinal metaplasia.
•  Men > women.
•  Increasing incidence with age.
•  Gland formation.
•  Hematogenous Spread.
•  Microsatellite instability.
•  APC gene mutations.
•  p53, p16 inactivation.
•  APC, adenomatous polyposis coli.

Diffuse
•  Blood group type A.
•  Women > men.
•  Younger age group.
•  Poorly differentiated,signet ring cells.
•  Transmural /lymphatic spread.
•  Decreased E-cadhedrin.
•  p53, p16 inactivation.