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

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 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) 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