Acute Gastritis
Acute Gastritis.
Pathological aspects of stomach-I
OBJECTIVES
By the end of the session the students should be able to:
a. Discuss Acute Gastritis.
b. Enlist the common causative agents in various age groups
c. Explain the pathogenesis and pathology
d. Enlist clinical features.
Normal Gastric mucosa
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Mucosa, Mucin &cytoprotection :
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Mucosa & synthesis of prostaglandins,
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The entire gastric mucosal surface is replaced every 2 to 6 days,
Formation of an “unstirred” layer of fluid that protects the mucosa.
PH of mucin layer is neutral as a result of HCO3+ secretion.
Prevents large food particles from directly touching the epithelium.
Prostaglandins enhance bicarbonate secretion.
Prostaglandins inhibit acid secretion.
Prostaglandins promote mucin synthesis.
Prostaglandins increase vascular perfusion.
Mucosa & acidity:
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The gastric lumen is strongly acidic with pH close to 1, > than a
1000,000 “million” times more acidic than the blood.
a. Discuss Acute Gastritis
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What is gastritis?
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Gastritis is an inflammation of the lining mucosa of the stomach. It is a
common disease that may occur in two forms:
[1] Acute form (Sudden or transient)
[2] Chronic form (prolonged).
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Acute gastritis:
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is a transient mucosal acute inflammatory process that may be
asymptomatic or cause variable degrees of clinical features:
{1} Epigastric pain. {2} Nausea. {3} Vomiting.
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Erosive Gastritis morphologically, when acute gastritis presents with
shallow erosions of the mucosa.
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Severe cases of acute gastritis- may be associated with:
{1} Mucosal erosion. {2} Ulceration. {3} Hemorrhage with
hematemesis and melena. {4} Rarely, massive blood loss.
The common causative agents in various age groups
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What are the most common causes of acute gastritis?
1. Heavy use of Aspirin (most common) and others NSAIDs.
2. Infection- H.pylori infection (Urease positive bacilli).
3. Sepsis (Streptococcal sepsis& Viral gastritis in immunosuppression)
e.g. CMV and Candida in AIDS patients
4. Excessive Alcohol consumption.
5. Heavy Smoking.
6.Stress (major surgery, burns and trauma).
7.Shock-related mucosa ischemia (burns, brain trauma, surgery).
8. Ingestion of acids and alkali (accidently, suicidal ingestion).
9. Parasitic: Anisakis (worm associated with eating raw fish) .
10. Radiation (radiotherapy), and chemotherapy.
11. Bile reflux gastritis and uremia
12. Mechanical trauma (nasogastric tube)
Mechanisms of Gastric injury and Protection
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Pathogenesis of Acute Gastritis
Erosions may develop because of:
1.
The direct effects of a potentially toxic substance
(e.g., alcohol, harsh chemicals=acids or bases).
2.
Reduced mucin synthesis as in the elderly.
3.
Hypoperfusion of the gastric mucosa in shock
(Mucosal cells more susceptible to the action of pepsin &HCL).
4.
Aspirin and NSAIDs inhibit the local synthesis of
prostaglandins & weaken mucosal defense system.
5. Radiation therapy, and chemotherapy (suppression of
growth, usually regenerate every 2 to 6 days).
6.
Decreased oxygen delivery .
Pathology of Acute Gastritis=Morphology
Four morphologic pattern:
1. Mild acute gastritis•
difficult to recognize.
2. Acute (Active) inflammation•
edema, congestion with neutrophilic infiltrates.
3. Gastric erosions•
erosions, exudate, fibrin, localized.
4. Acute erosive hemorrhagic gastritis•
When wide area of erosions with hemorrhage, may progress
to ulcer.
Ulcer vs. Erosion of GIT
Ulcer = Necrosis (or breach) involving the entire
thickness of the mucosa that extend through the
muscularis mucosa into the submucosa or deeper
Erosion= Necrosis (or breach) involving only the
superficial mucosa.
Morphology Active inflammation (Acute Gastritis)
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1. Gross: diffusely hyperemic
gastric mucosa.
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2. Microscopic:
{A} The surface epithelium&
glands: is intact with scattered
neutrophils among the epithelial cells
“intraepithelial” or within mucosal
glands.
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{B}The lamina propria: moderate
edema & vascular congestion.
Morphology of Acute erosive hemorrhagic gastritis
1.
2.
Define as concurrent erosions
and hemorrhage,
Hyperemic mucosa
3.
Large areas of the gastric
surface erosions, the
involvement is typically
superficial.
4.
Pronounced neutrophilic.
Fibrin-containing purulent
exudate in the lumen
Ulcer: erosions may progress
to ulcers.
5.
6.
Clinical features of Acute gastritis
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Most critically ill patients admitted to hospital ICU.
1.Asymptomatic.
2.Epigastric
pain.
3.Nausea.
4.Vomiting.
5.Bleeding
from superficial gastric erosions or ulcers that
may require transfusion (Gastric Mucosal damage).
Hemtamesis and melena.
Rarely, massive blood loss.
6. Others Complications of Gastric ulcer:
 Bleeding.
 Perforation.
 Obstruction.
ACUTE GASTRIC ULCERATION
The etiological factors of acute gastric ulceration are::
1.
Well-known complication of therapy with NSAIDs.
2.
Severe physiologic stress.
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Types of acute gastric ulceration: given specific names,
based on location and clinical associations:
A.
Stress ulcers: shock, sepsis, or severe trauma. (Stomach).
Cushing ulcers- occurs Gastric, duodenal, and esophageal
ulcers arising in persons with CNS injury with intracranial
disease, carry a high incidence of perforation.
NB: Curling ulcers: (Proximal duodenum), a\w Burn or trauma.
B.
Acute gastric ulceration-Pathogenesis
1.
2.
is complex & not well-understood.
NSAID-induced ulcers are related to cyclooxygenase
inhibition This prevents synthesis of prostaglandins.
Lack of prostaglandins synthesis lead to:
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Deceased bicarbonate secretion.
Reduced mucin synthesis.
Reduced mucosal vascular perfusion.
3.
Lesions associated with intracranial injury- caused by
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direct stimulation of vagal nuclei, which lead to:
Hypersecretion of gastric acid.
Systemic acidosis evoke gastric acid secretion& damage to
the cells.
Hypoxia and reduced blood flow caused by stress-induced
splanchnic vasoconstriction.
Acute gastric ulceration-Morphology
Macroscopic:
1.
Site: anywhere in the stomach
2.
Shape: irregular, rounded.
3. Size:
< than 1 cm diameter.
4.
Number: Singly, often multiple
5.
Margins: not indurated.
6.
Base: stained brown to black
by acid digestion of extravasated blood.
Acute gastric ulceration-Morphology
Microscopic:
1.
Sharply demarcated& shallow.
2.
Transmural inflammation + Serositis.
3.
Suffusion of blood into the mucosa
and submucosa.
4.
Absent scarring& thickening of blood
vessels “chronic peptic ulcers”
** Healing with re-epithelialization, will
take place within days to several
weeks.
Questions ??