Gastritis

Gastritis
Pre by MR.ZAHID REHMAN

IPMS(KMU)
Anatomy of stomach
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
5
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.
 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.
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
Protective factors vs. hostile factors
Gastritis
Acute Chronic
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
Acute Gastritis
Definition
An acute mucosal inflammatory
process, with neutrophilic
infiltrate, that is usually transient.
There may be hemorrhage into
the mucosa.
Severe erosive form is an
important cause of severe GI
bleeding
Etiology
heavy use of NSAIDS, especially

aspirin
excessive alcohol consumption
heavy smoking
severe stress e.g. trauma, burns,
surgery
Ischemia
Systemic infection
Often, idiopathic
NSAIDs
NSAIDs and aspirin also
interfere with the protective
mucus layer by inhibiting
mucosal cyclooxygenase activity,
reducing levels of mucosal
prostaglandins
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
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
Acute Gastritis -
Pathogenesis
Acid secretion + Bicarbonate

All above Factor
+ back diffusion buffer
Direct Disruption
Mucosal + of Blood flow
Injury Mucus layer
Acute Gastritis
ACUTE GASTRITIS - MORPHOLOGY
Mucosal
congestion ,edema
inflammation & ulceration
Acute Gastritis
diffusely hyperemic
gastric mucosa
 causes for acute
gastritis
alcoholism
drugs
infections, etc.
Acute Gastritis
Clinical Features
 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
Complications:
Malignancy
Hemorrhage
Perforation
Obstruction
Chronic Gastritis
Definition
Chronic mucosal inflammatory changes leading

to atrophy and metaplasia .
Dysplasia and ultimate neoplasia are

complications.
Chronic Gastritis
Type A
Type B
Autoimmune
Antral Gastritis
gastritis
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
H. pylori Gastritis - Morphology
H. pylori organisms along

superficial mucus layer of
antral biopsy
Web Path
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
Clinical feature
 nausea
 vomiting
 upper abdominal discomfort
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
Autoimmunity
(>10%): Antibodies to parietal cells cause
parietal cell destruction (HCl & intrinsic factor)
Autoimmune  diffuse mucosal damage of the body-

fundic mucosa

Gastritis

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Gastritis

Pre by MR.ZAHID REHMAN

 acid production or pepsin

Acute refers to short term inflammation

Chronic referring to long standing forms

heavy use of NSAIDS, especially

Diet and Stress Action

Diet Dyspepsia, may  pain - not believed

Physiologic ↓ mucosal blood flow, tissue hypoxia,

Acid secretion + Bicarbonate

Chronic mucosal inflammatory changes leading

Dysplasia and ultimate neoplasia are

H. pylori organisms along

The effect of bile salts on gastric mucosa is

Autoimmune  diffuse mucosal damage of the body-

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