essay 29 - gastritis and ulcers - etiology, pathogensis, types

how is the gastrodudodenal mucosa maintained by balancing between?

• protective factors = mucus layer, prostaglandins, adequate blood flow, cell renewal, growth factors

• damaging factors = H. pylori, NSAIDs, ethanol, bile acids, smoking, ischemia, hypoxia, stress

• disease occurs when damaging factors outweigh protective mechanisms

what is gastritis

• inflammation of gastric mucosa, which may be acute (sudden, reversible) or chronic (persistent, with risk of atrophy)

classifications of gastritis

1. by onset

• acute gastritis - sudden, caused by irritants, drugs, alcohol, stress, infecttions)

• chronic gastritis - progressive, linked to H. pylori or autoimmune destruction

2. by location

• type A - fundic (autoimmune)

• type B - antral (H. pylori)

• Type AB - pangastritis (fundus + antrum)

etioology of gastritis

• Environmental = smoking, radiation

• dietary = alcohol, spicy food

• pathophysiologic success= shock, burns (curlings ulcers), liver failure, renal failure

• drugs = NSAIDs, corticosteroids, some antibiotics

• other = psychological stress, autoimmune disorders

• H. pylori = most common cause of chronic gastritis

pathogenesis of gastritis

• acute gastritis = disruption of mucosal barrier allowing gastric acid and digestive enzymes to damage the endothelial lining causing inflammation

• Chronic gastritis=
  1. H. pylori gastritis:
  - produces urease → converts urea → ammonia → neutralised acid for survival, but injured mucosa
  - toxins, lipases, proteases → direct cytotoxicity
  - inflammatory response → chronic damage → risk of ulcers and carcinoma
  2. Autoimmune gastritis (atrophic)
  - autoantibodies against parietal cells and intrinsic factor
  - loss of HCL and intrinsic factor → achlorhydria and B12 malabsorption → pernicious anaemia
  - long standing inflammation → precancerous state (adenocarcinoma risk)

clinical manifestations of gastritis

• acute= anorexia, nausea, vomiting, epigastric pain, hematemesis (esp. with alcohol abuse)

• chronic = dyspepsia, bloating, glossitis (with B12 deficiency), progressive atrophy → risk of carcinoma

describe peptic ulcer disease (PUD) and the types

• a defect in the gastric or duodenal mucosa that penetrates the muscularis mucosa into submucosa or deeper. Precancerous condition (esp. gastric ulcer)

• Type I - primary gastric ulcer (antral gastritis)

• Type II - gastric + duodenal ulcers

• Type III - prepyloric ulcers

• Type IV - cardia/proximal stomach ulcers

• Type V - anywhere (NSAID-related)

• By morphology:
  - acute ulcer = smooth borders, clean base, may cause severe GI bleeding
  - chronic ulcers - raised, fibrotic borders, inflamed based, most common form

etiology of ulcers

• aggressive factors = H. pylori, hyperacidity (e..g zollinger-ellison syndrom), pepsin, smoking, caffeine

• weakened defences = NSAIDs (block prostaglandins), corticosteroids, alcohol, stress, bile reflex

pathogenesis of ulcer formation

1. increased vagal stimulation or instrinsice hyperactivity → parietal cell hyperplasia → increased HCI secretion

2. acid+pepsin injure mucosa (esp duodenum)

3. defenses (mucus, bicarbonate, blood flow) are overwhelmed or inhibited

4. H. pylori worsens by:
   - urease → ammonia → epithelail injury
   - toxins + enzymes → mucosal breakdown
   - chronic inflammation _> impaired healing

5. result → focal mucosal erosin → ulceration into deeper layers

clinical features of ulcers

1. gastric ulcers

• less common

• pain during or shortly after meal

• anorexia, nausea, weightless

2. duodenal ulcer

• more common

• pain 2-3 hours after meals, relived by food

• good appetite, often well nourished, nocturnal pain

complications of gastritis and ulcers

• bleeding, anaemia, haemorrhage, hypovolemic shock

• perforation or penetration (into pancreas)

• pyloric stenosis (scarring)

• progression to peptic ulcer, carcinoma or lymphoma