diseases of the stomach prof: hussien gadalla. gastric disorders acute gastritis chronic gastritis...
TRANSCRIPT
Diseases of The Stomach
Prof:Hussien Gadalla
Gastric Disorders
• 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
GastritisEtiology and Pathophysiology
• Risk factors (cont’d)– Environmental factors
• Radiation, smoking
– Pathophysiologic conditions• Burns, renal failure, sepsis
– Other factors• Psychologic stress, NG tube
Pathogenesis
• 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 pylori 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)
metaplasiaSeen 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