Transcript Diseases of The Stomach

Diseases of The Stomach
Prof:
Hussien Gadalla
Gastric Disorders
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Acute Gastritis
Chronic Gastritis
Peptic Ulcer Disease
These three are common and related
disorders.
Defences of Stomach
• Mucosal barrier: which comprises mucus which is
alkaline and tight intercellular junctions to prevent
acid from penetrating
• Good gastric blood flow
• High rate of gastric mucosal turnover
• Prostaglandins which stimulate secretion of mucus
(reduced by COX1 inhibition)
Acute Gastritis
• It is an acute mucosal inflammatory process
• Risk factors
– Drugs
• Direct irritating effect on gastric mucosa
• Aspirin, NSAIDs, and corticosteroids
– Diet
• Alcohol, spicy food
-- Systemic infection: salmooellosis
Gastritis
Etiology and Pathophysiology
• Risk factors (cont’d)
– Environmental factors
• Radiation, smoking
– Pathophysiologic conditions
• Burns, renal failure, sepsis
– Other factors
• Psychologic stress, NG tube
Pathogenesis
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One or more of the following may play a role:
Direct damage to the epithelium
Disruption of the adherent mucous layer.
Stimulation of acid secretion with back diffusion
of hydrogen ions into the superficial layer.
• Decreased production of bicarbonate buffer by
the superficial epithelium
• Reduced mucosal blood flow
Acute gastritis
• A cute erosion (loss of
mucosa superficial to
muscularis mucosae). Can
result in severe
haemorrhage
• Acute Helicobacter
infection has a prominent
neutrophil infiltrate
Chronic gastritis
• Chronic gastritis is defined as the presence of
chronic mucosal inflammatory changes
leading eventually to mucosal atrophy and
epithelial metaplasia.
• A – Bacterial (helicobacter)
• B – Autoimmune
• C - Chemical
Chronic Gastritis
• Risk factors (cont’d)
– Microorganisms
• Helicobacter pylori
– Important cause of chronic gastritis
– Promotes breakdown of gastric mucosal barrier
• Staphylococcus organisms
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
Pathogenesis
• Factors permitting colonisation:
• (i) Spiral shape and flagellate – for motility within
this mucous layer.
• (ii) Urease activity – which generate ammonium
ions that buffer gastric activity
• (iii) Micro-aerophilism – for survival within the
mucous gel
• (iv) Attachment to epithelial cells
• (v) Evasion of Immune response
Figure 2. Pathogen–Host Interactions in the Pathogenesis of Helicobacter pylor
Infection.
Helicobacter gastritis
• Acute inflammation
mediated by complement
and cytokines
• Polymorphisms infiltrate
epithelium and may be
partly responsible for its
destruction
• An immune response is
also initiated (antibodies
may be detected in
serum)
Figure 3. Natural History of Helicobacter pylori Infection.
Chronic Gastritis
• Risk factors (cont’d)
– Autoimmune atrophic gastritis
• Affects fundus and body of stomach
• Associated with increased risk of gastric cancer
• May be link to presence of H. pylori and development
of autoimmune chronic gastritis
Autoimmune chronic gastritis
• Autoantibodies to gastric parietal cells
• Hypochlorhydria/achlorhydria
• Loss of gastric intrinsic factor leads to
malabsorption of vitamin B12 with
macrocytic,megaloblastic anaemia
Morphology of chronic gastritis
• Chronic inflammatory cell
infiltration
• Mucosal atrophy
• Intestinal (goblet cell)
metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
Chemical gastritis
• Commonly seen with bile
reflux (toxic to cells)
• Prominent hyperplastic
response (inflammatory
cells scanty)
• With time – intestinal
metaplasia