Diseases of The Stomach

1
Diseases of The Stomach

• Prof
• Hussien Gadalla

2
Gastric Disorders

• Acute Gastritis
• Chronic Gastritis
• Peptic Ulcer Disease
• These three are common and related disorders.

3
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)

4
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

5
GastritisEtiology and Pathophysiology

• Risk factors (contd)
• Environmental factors
• Radiation, smoking
• Pathophysiologic conditions
• Burns, renal failure, sepsis
• Other factors
• Psychologic stress, NG tube

6
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

7
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

8
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

9
Chronic Gastritis

• Risk factors (contd)
• Microorganisms
• Helicobacter pylori
• Important cause of chronic gastritis
• Promotes breakdown of gastric mucosal barrier
• Staphylococcus organisms

10
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

11
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

12
Figure 2. PathogenHost Interactions in the
Pathogenesis of Helicobacter pylori Infection.
13
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)

14
Figure 3. Natural History of Helicobacter pylori
Infection.
15
Chronic Gastritis

• Risk factors (contd)
• 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

16
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

17
Morphology of chronic gastritis

• Chronic inflammatory cell infiltration
• Mucosal atrophy
• Intestinal (goblet cell) metaplasia
• Seen in Helicobacter and autoimmune gastritis
  (not chemical)

18
Chemical gastritis

• Commonly seen with bile reflux (toxic to cells)
• Prominent hyperplastic response (inflammatory
  cells scanty)
• With time intestinal metaplasia