9. Definition
The term gastritis is used to denote
inflammation associated with
mucosal injury.
Gastritis is mostly a histological term that
needs biopsy to be confirmed.
Gastritis is usually due to infectious
agents (such as Helicobacter pylori) and
autoimmune and hypersensitivity
reactions.
10. Definition
Epithelial cell damage and regeneration
without associated inflammation is
properly referred to as "gastropathy.―
Gastropathy may be referred without
histological evidence and just according to
gross appearance in endoscopy or radiology
Gastropathy is usually caused by irritants such
as drugs (e.g., nonsteroidal anti-inflammatory
agents and alcohol), bile reflux, hypovolemia,
and chronic congestion.
11. Sex:
Male-to-female ratio of gastritis is approximately1:1
Male-to-female ratio of PUD is approximately 2:1
12. 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
15. 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
16. 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
17. 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
18. NSAIDs
NSAIDs and aspirin also
interfere with the protective
mucus layer by inhibiting
mucosal cyclooxygenase activity,
reducing levels of mucosal
prostaglandins
19. 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
20. Effects of Diet and Stress
Diet and Stress Action
Diet Dyspepsia, may pain - not believed
to cause ulcer or assist healing
Physiologic ↓ mucosal blood flow, tissue hypoxia,
stress mucosal lining degradation; e.g. ICU,
sepsis, burn, trauma. Associated with
multiple erosions & significant bleeding
22. Acute Gastritis - Pathogenesis
Acid secretion + Bicarbonate
All above Factor
+ back diffusion buffer
+
Direct Disruption
Mucosal + of Blood flow
Injury Mucus layer
Acute Gastritis
23. Stages of Acute Gastritis
Acute superficial Acute erosive
gastritis gastritis
Inflammation of Destruction of multiple
superficial gastric small zones of
mucosa. superficial mucosa.
Acute Gastric Ulceration
Destruction of full thickness of mucosa
25. 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.
26. Acute Gastritis
Gastric mucosa
demonstrates
infiltration by
Neutrophils
27. Acute Gastritis
diffusely hyperemic
gastric mucosa
causes for acute
gastritis
alcoholism
drugs
infections, etc.
28. Acute Gastritis
Clinical Features
broad range of signs and symptoms that depend
on the severity of the condition
Asymptomatic
Epigastric pain, nausea & vomiting
Hemorrhage, massive hematemesis, melena, or
fatal blood loss
One of the major causes of massive
hematemesis, particularly in alcoholics.
~25% patients taking aspirin for rheumatoid
arthritis will develop acute gastritis, and some
will bleed
30. Chronic Gastritis
Definition
Chronic mucosal inflammatory changes leading
to atrophy and metaplasia (usually without
erosions)
Dysplasia and ultimate neoplasia are
complications.
31. Chronic
Gastritis
Type B Type A
Antral Autoimmune
Gastritis gastritis
32. 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)
33. 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)
34. Helicobacter pylori
Adapted to live in
association with
surface epithelium
beneath mucus barrier
Causes cell damage
and inflammatory cell
infiltration
In most countries the
majority of adults are
infected
35. H. pylori Gastritis - Morphology
H. pylori organisms along
superficial mucus layer of
antral biopsy
Web Path
36. Bile reflux gastropathy
Bile reflux gastropathy typically results from the
regurgitation of bile into the stomach because
of an operative stomach, an incompetent
pyloric sphincter, or abnormal duodenal motility.
The effect of bile salts on gastric mucosa is
comparable to that seen after chronic NSAID
use
37. Chemical gastritis
Commonly seen with bile
reflux (toxic to cells)
Prominent hyperplastic
response (inflammatory
cells scanty)
With time – intestinal
metaplasia
38. Clinical Features
Usually only a few symptoms:
nausea, vomiting, upper abdominal discomfort
Most infected person have gastritis, but
are asymptomatic
Hypochlorhydria, but NOT achlorhydria
and pernicious anemia (parietal cells
never completely destroyed)
Gastrin normal to slightly elevated
Antibiotics are treatment of choice
39. Clinical Complications
H. pylori
H. pylori predisposes to peptic ulcers
in duodenum and stomach—Most
patients with a peptic ulcer are
infected.
Risk of gastric carcinoma and
lymphoma
40. 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
41. Morphology of chronic gastritis
Chronic inflammatory cell
infiltration
Mucosal atrophy
Intestinal (goblet cell)
metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
42. 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.
44. 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
45. 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)
46. 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)
47. 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
48. Hypertrophic gastritis
Three variants are recognized
Menetrier’s disease
Hypersecretory gastropathy
Gastric gland hyperplasia
[the Zollinger-Ellison syndrome]
50. Ménétrier's disease
Epithelial hyperplasia
involving the surface
and foveolar mucous
cells (i.e., foveolar
hyperplasia); the
oxyntic glands can be
normal or atrophic.