My Clinical Notes

• Defined histologically as a breach in the mucosa of the alimentary tract that extends through the muscularis mucosa into the submucosal or deeper
• May occur anywhere in the GIT, but occur most commonly in the stomach and duodenum (80%)
• Ulcers differ from erosions, in which there is epithelial disruption but no breach in the muscularis mucosa

 

Peptic Ulcers

 

• Chronic typically solitary ulcers that arise from exposure to acid-peptic secretion

 

Epidemiology

• Lifetime likelihood of developing a peptic ulcer in the US is 10% for men and 4% for females
• Typically diagnosed in middle aged and older people
• Women most commonly affected at or after menopause for unknown reasons
• There has been a significant decreased in the prevalence of duodenal ulcers over the past decades but not gastric ulcers
• There are no apparent genetic tendencies

 

Pathogenesis

• Produced by an imbalance between gastroduodenal mucosal defence and the damaging forces particularly gastric acid and pepsin
• Hyperacidity is less common than failure of mucosal defences;
  • Ischaemia and shock – reduced blood flow
  • Delayed gastric emptying
  • Duodenal-gastric reflux
• Most peptide ulcers are associated with H.pylori – present in 70% of gastric ulcers and virtually all patient with duodenal ulcers
• H. pylori causes injury by the following mechanisms
  • Secretion of urease, proteases and phosholipases which can directly damage the mucosa
  • Stimulation of proinflammatory cytokine production by mucosal cells which recruits and activates inflammatory cells which in turn can release proteases and ROI
  • Bacterial platelet activating factor which promotes capillary thrombosis
  • Damage to the mucosa permits nutrient leakage onto the surface environment thus sustaining the bacillus in the mucus layer
  • H.pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum, this can result in gastric metaplasia of the duodenum providing another area of colonisation of the bacteria

 

• Of those infected world wide only 10-20% actually develop an ulcer

 

• Other events either alone or in concert with H.pylori may promote peptic ulceration;
  • Hyperacidity – increased parietal cell mass from excess gastrin production e.g. gastroma causing multiple peptic ulcerations (Zollinger Ellison syndrome)
  • Chronic NSAID use suppressing mucosal prostaglandin synthesis
  • Cigarette smoking impairs blood flow and healing
  • Alcoholic cirrhosis
  • Corticosteroids
  • Hypercalcaemia stimulates gastrin secretion

 

Morphology

• 98% of ulcers occur in the duodenum and stomach (4:1)
• Gross findings include a sharply punched out border with overhanging mucosal borders and a smooth, clean ulcer bases
• Microscopically there may be 4 areas;
  • Thin superficial layer of necrotic debris
  • Underlying non specific inflammatory infiltrate predominately neutrophils
  • In the deeper layers there may be granulation tissue infiltrated with mononuclear cells
  • This may develop into a more solid fibrous or collagenous scar
• The surrounding mucosa generally exhibits chronic gastritis

 

Clinical

• The majority cause epigastric gnawing, burning or aching pain
• Worse at night and 1-3 hours after a meal
• Nausea, vomiting, bloating, belching occur along with weight loss
• Complications include;
  • Anaemia
  • Haemorrhage
  • Perforation
  • Obstruction
• Malignant transformation is rare and related to underlying gastritis

 

Acute Gastric Ulceration

 

• Refers to focal, acute mucosal defects in the setting of severe stress
• May be also be caused by NSAIDs which decrease mucosal prostaglandins
• Multiple lesions mainly in the stomach and occasionally in the duodenum
• Stress erosions are more commonly encountered in patients with;
  • Shock
  • Extensive burns
  • Sepsis
  • Severe trauma
  • Raised ICP
  • Following intracranial surgery
• Those associated with severe burns or trauma are called Curling ulcers
• Those arising following intracranial injury or operations are called Cushing ulcers and carry a high incidence of perforation. Possibly due to direct stimulation of vagal nuclei leading to hypersecretion of gastric acid
• Other pathogenesis is unclear, possibly impaired oxygenation and systemic acidosis play a role

 

Morphology

• Ulcers are generally less than 1cm in diameter, multiple and shallow
• The ulcer base is brown due to acid digestion of extruded blood
• Adjacent mucosa is normal

 

Clinical

• Acute gastric erosions or ulcers occur in 5-10% of ICU patients
• The single most important determinant of outcome in the ability to correct the underlying cause

 

This entry was posted on Sunday, February 24th, 2008 at 1:57 pm and is filed under Gastrointestinal. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.