I m a student of BEMS 4th Professional at University of Poonch. Sir Asif teach us Pathology.

2. Aamir Sharif,
BEMS 4th Professional
Department of Eastern Medicine & Surgery

3. Stomach
 3 muscle layers
 Oblique
 Circular
 Longitudinal
 Regions
 Cardiac sphincter
 Fundus
 Antrum (pylorus)
 Pyloric sphincter
 Vascular
 Inner surface thrown into
folds – Rugae
 Contains enzymes that work
best at pH 1-2 3

4. Normal Stomach Anatomy

5. Stomach - Normal

6. Stomach - Normal

7. Stomach
 Functions  Absorbs
 Mix food  Alcohol
 Reservoir  Water
 Start digestion of
 Lipophilic acid
 Protein
 B 12
 Nucleic acids
 Fats
 Activates some enzymes
 Destroy some bacteria
 Makes intrinsic factor – B
12 absorption
 Destroys some bacteria
7

8. Inflammatory
Disease of Stomach

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

13. Protective factors vs. hostile factors

14. Gastritis
Acute Chronic

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

21. Etiology of
Gastritis
A) Normal
B) Increased
Attack
*Hcl
*Pepsin.
*NSAIDs.
C) Weak defense
*Helicobacter pylori
*Stress, drugs, smoking

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

24. ACUTE GASTRITIS -
MORPHOLOGY
Mucosal congestion ,edema
inflammation & ulceration

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

29. Complications:
 Malignancy
 Hemorrhage
 Perforation
 Obstruction

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.

43. Autoimmune Gastritis -Morphology
Diffuse mucosal damage of the body and fundic
mucosa. Antrum less involved.
PJ Goldblatt, MD

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]

49. Hyperplastic gastropathies
proliferative,
inflammatory, and
infiltrative
conditions are
associated with
large folds due to
excessive number
of mucosal
epithelial cells

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.

51. Zollinger-Ellison syndrome
Increased numbers
of parietal cells
with no change in
surface and
foveolar mucous
cells.

52. Hyperplastic gastropathies
mixed-type in which
both mucous and
oxyntic glandular
cells show
hyperplasia, may be
seen in as
lymphocytic and H.
pylori gastritis.

53.  Stomach
 Acute Gastritis= inflammation of gastric mucosa
 acute – presence of neutrophils
 Chronic –lymphocytes and plasma cells
 Caused by ingestion of strong acids or alkalies, NSAIDs,
cancer chemotherapy, irradiation, alcohol, uremia, severe
stress & shock states
 Proposed mechanisms: ↑ acid production with ↓ surface
bicarbonate buffer
 Morphology: Mucosal edema, hyperemia, PML infiltration,
erosions (not deeper than muscularis mucosa) &
hemorrhages

54.  Stomach
 Chronic Gastritis = Chronic mucosal inflammation
 Leading to mucosal atrophy, intestinal metaplasia &
dysplasia.
 Pathogenesis:
 Chronic infection by Helicobacter pylori (90%): MCC of
chronic gastritis, Elaboration of urease  produces
ammonia that buffers gastric acid, protecting organism from
acid
 Other diseases associated with H. pylori Infection
 Peptic ulcer disease
 Gastric carcinoma
 Gastric lymphoma
 Autoimmunity (>10%): Antibodies to parietal cells cause
parietal cell destruction (HCl & intrinsic factor)

55.  Stomach
 Chronic Gastritis
 Morphology:
 Autoimmune diffuse mucosal damage of the body-fundic
mucosa
 H. pylori affect antral mucosa
 Histology: Lymphocytic & plasma cell infiltrate of the lamina propria
 atrophy, regeneration, metaplasia (to intestinal type mucosa) &
dysplasia.
 H. pylori detected on the mucosal surface
 Clinically:
 Mild abdominal discomfort, nausea, vomiting; hypochlorhydria,
hypergastrinemia & rarely
 Overt pernicious anemia (in autoimmune) gastritis).
 Long-term risk of cancer is 2-4%