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Gastritis
Raika Jamali M.D.
Gastroenterologist and hepatologist
Sina Hospital
Tehran University of Medical Sciences
● Histologically documented inflammation of
the gastric mucosa
● There is no typical clinical manifestation of
gastritis
●
inflammation and atrophy in different types of
atrophic
and nonatrophic chronic gastritis
Acute Gastritis
● Most common causes of acute gastritis
are infectious (H. pylori )
● Sudden onset of epigastric pain, nausea,
and vomiting
● If not treated, this picture will evolve into
one of chronic gastritis
● Phlegmonous gastritis is a rare (Elderly
individuals, alcoholics, and AIDS )
● Failure of supportive measures and
antibiotics may result in gastrectomy
● Herpes simplex or CMV gastritis in AIDS
Chronic Gastritis
● Inflammatory cell infiltrate consisting
primarily of lymphocytes and plasma cells
● Distribution of the inflammation may be
patchy, initially involving superficial and
glandular portions of the gastric mucosa.
● This picture may progress to more severe
glandular destruction, with atrophy and
metaplasia
Superficial gastritis
● The early phase of chronic gastritis
● Inflammatory changes are limited to the
lamina propria of the surface mucosa, with
edema and cellular infiltrates separating
intact gastric glands
● Decreased mucus in the mucous cells and
decreased mitotic figures in the glandular
cells
Atrophic gastritis
● Inflammatory infiltrate extends deeper into
the mucosa, with progressive distortion
and destruction of the glands
● Final stage of chronic gastritis is gastric
atrophy
● Endoscopically, the mucosa may be
substantially thin, permitting clear
visualization of the underlying blood
vessels
● Gastric glands may undergo morphologic
transformation in chronic gastritis.
● Intestinal metaplasia denotes the
conversion of gastric glands to a small
intestinal phenotype with small-bowel
mucosal glands containing goblet cells.
● The metaplastic changes may vary in
distribution from patchy to fairly extensive
gastric involvement.
● Intestinal metaplasia is an important
predisposing factor for gastric cancer
● Chronic gastritis is also classified
according to the predominant site of
involvement:
● Type A refers to the body-predominant
form (autoimmune)
● Type B is the antral-predominant form (H.
pylori–related).
Type A Gastritis
● less common
● Involves primarily the fundus and body
● Antral sparing
● Associated with pernicious anemia
● Antibodies against parietal cells and IF
(autoimmune gastritis)
● H. pylori infection can lead to a similar
distribution of gastritis
●
● Antibodies to parietal cells have been
detected in >90% of patients with
pernicious anemia
● in up to 50% of patients with type A
gastritis
● Parietal cell antibodies and atrophic
gastritis are observed in family members
● half of patients with pernicious anemia
have antibodies to thyroid antigens
● ~ 30% of patients with thyroid disease
have circulating antiparietal cell antibodies
● Anti-IF antibodies are more specific than
parietal cell antibodies
● HLA-B8 and -DR3
● Achlorhydria & vitamin B12 deficiency
results
● Sparing of the antral mucosa (site of G
cells), leads to hypergastrinemia
● Development of gastric carcinoid tumors
Type B Gastritis
● The more common form
● H. pylori is the cause
● Improves after H. pylori eradication
● antral-predominant, gastritis
● Progression of the inflammatory process
toward the body and fundus
● Conversion to a pan-gastritis is
time-dependent–estimated to require
15–20 years
● Number of H. pylori organisms decreases
dramatically with progression to gastric atrophy,
● Degree of inflammation correlates with the level
of these organisms
● Multifocal atrophic gastritis, gastric atrophy with
subsequent metaplasia
● lead to development of gastric adenocarcinoma
or low-grade B cell lymphoma (gastric MALT
lymphoma)
● Eradication of H. pylori as a general preventative
measure for gastric cancer is being evaluated
but is not yet recommended
Treatment
● Patients with pernicious anemia will
require parenteral vitamin B12
supplementation on a long-term basis.
●
● Eradication of H. pylori is not routinely
recommended unless PUD or a low-grade
MALT lymphoma is present

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Gastritis.ppt.pdf

  • 1. Gastritis Raika Jamali M.D. Gastroenterologist and hepatologist Sina Hospital Tehran University of Medical Sciences
  • 2. ● Histologically documented inflammation of the gastric mucosa ● There is no typical clinical manifestation of gastritis ●
  • 3.
  • 4. inflammation and atrophy in different types of atrophic and nonatrophic chronic gastritis
  • 5. Acute Gastritis ● Most common causes of acute gastritis are infectious (H. pylori ) ● Sudden onset of epigastric pain, nausea, and vomiting ● If not treated, this picture will evolve into one of chronic gastritis ● Phlegmonous gastritis is a rare (Elderly individuals, alcoholics, and AIDS ) ● Failure of supportive measures and antibiotics may result in gastrectomy ● Herpes simplex or CMV gastritis in AIDS
  • 6. Chronic Gastritis ● Inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells ● Distribution of the inflammation may be patchy, initially involving superficial and glandular portions of the gastric mucosa. ● This picture may progress to more severe glandular destruction, with atrophy and metaplasia
  • 7. Superficial gastritis ● The early phase of chronic gastritis ● Inflammatory changes are limited to the lamina propria of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands ● Decreased mucus in the mucous cells and decreased mitotic figures in the glandular cells
  • 8. Atrophic gastritis ● Inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands ● Final stage of chronic gastritis is gastric atrophy ● Endoscopically, the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels
  • 9. ● Gastric glands may undergo morphologic transformation in chronic gastritis. ● Intestinal metaplasia denotes the conversion of gastric glands to a small intestinal phenotype with small-bowel mucosal glands containing goblet cells. ● The metaplastic changes may vary in distribution from patchy to fairly extensive gastric involvement. ● Intestinal metaplasia is an important predisposing factor for gastric cancer
  • 10. ● Chronic gastritis is also classified according to the predominant site of involvement: ● Type A refers to the body-predominant form (autoimmune) ● Type B is the antral-predominant form (H. pylori–related).
  • 11. Type A Gastritis ● less common ● Involves primarily the fundus and body ● Antral sparing ● Associated with pernicious anemia ● Antibodies against parietal cells and IF (autoimmune gastritis) ● H. pylori infection can lead to a similar distribution of gastritis ●
  • 12. ● Antibodies to parietal cells have been detected in >90% of patients with pernicious anemia ● in up to 50% of patients with type A gastritis ● Parietal cell antibodies and atrophic gastritis are observed in family members ● half of patients with pernicious anemia have antibodies to thyroid antigens ● ~ 30% of patients with thyroid disease have circulating antiparietal cell antibodies
  • 13. ● Anti-IF antibodies are more specific than parietal cell antibodies ● HLA-B8 and -DR3 ● Achlorhydria & vitamin B12 deficiency results ● Sparing of the antral mucosa (site of G cells), leads to hypergastrinemia ● Development of gastric carcinoid tumors
  • 14. Type B Gastritis ● The more common form ● H. pylori is the cause ● Improves after H. pylori eradication ● antral-predominant, gastritis ● Progression of the inflammatory process toward the body and fundus ● Conversion to a pan-gastritis is time-dependent–estimated to require 15–20 years
  • 15. ● Number of H. pylori organisms decreases dramatically with progression to gastric atrophy, ● Degree of inflammation correlates with the level of these organisms ● Multifocal atrophic gastritis, gastric atrophy with subsequent metaplasia ● lead to development of gastric adenocarcinoma or low-grade B cell lymphoma (gastric MALT lymphoma) ● Eradication of H. pylori as a general preventative measure for gastric cancer is being evaluated but is not yet recommended
  • 16. Treatment ● Patients with pernicious anemia will require parenteral vitamin B12 supplementation on a long-term basis. ● ● Eradication of H. pylori is not routinely recommended unless PUD or a low-grade MALT lymphoma is present