OF PEPTIC ULCER

   Ulcers are defined as a breach in the mucosa of the
    alimentary tract, which extends through the muscularis
    mucosa into the submucosa or deeper.

    ( An erosion differs from an ulcer in being partial
     thickness mucosal defect).

   Peptic ulcers are chronic most often solitary, lesions that
    occur in any portion of gastrointestinal tract exposed to
    the aggressive action of acid-peptic juices.
Clinical presentation:

   Remitting, relapsing lesion
   Most often diagnosed in middle aged to older adults but
    may first become evident in young adult life.
   Epigastric burning or aching pain.
   Pain worse at night and 1 to 3 hours after meal.
   Nausea, vomiting, bloating , belching and weight loss
   Complication: Anaemia, hemorrhage, perforation,
    obstruction. Malignant formation is rare and related to
    underlying gastritis.
Sites of peptic ulcer:

   Duodenum: First portion ( few cms from the pyloric ring).
    Anterior wall is more often affected.
   Stomach: Usually antrum. Lesser curvature (common) .
    Anterior and posterior wall and greater curvature (less
   In the margins of a gastroenterostomy (stomal ulcer)
   In the duodenum, stomach or jejunum of patients with
    Zollinger-Ellison syndrome.
   Within or adjacent to a Meckel’s diverticulum that
    contains ectopic gastric mucosa.
Pathogenesis of peptic ulcer:    ( see diagram )

 Peptic ulcers are produced by an imbalance
 between the gastro-duodenal mucosal defense
 mechanisms and damaging forces of gastric
 acid and pepsin, combined with superimposed
 injury from environmental or immunologic
Role of H. Pylori infection in the pathogenesis of peptic
  H. pylori infection is present in almost all patients with duodenal
   ulcers and 70% cases with gastric ulcers.
  Duodenal ulcers - Usually associated with gastritis confined to
   the antrum.
  Gastric ulcers - Usually associated with pangastritis.
 H. pylori secretes urease (generates ammonia), protease (breaks
   down glycoprotein in the gastric mucus) or phospholipases.
 Bacterial lipopolysaccharide attracts inflammmatory cells to
   the mucosa. Neutrophils release myeloperoxide.
   A bacterial platelet-activating factor promotes thrombotic
   occlusion of surface capillaries.
 Mucosal damage allows leakage of tissue nutrients in the
   surface microenvironment , sustaining the bacillus.
H. Pylori infection in peptic ulceration: (continued)

   Damage of the protective mucosal layer. The epithelial cells are
    exposed to the damaging effect of acid-peptic digestion.
   Inflammation of the gastric mucosa.
   Chronically inflamed mucosa more susceptible to acid- peptic
    injury and prone to peptic ulceration.
    Ulcers occur at sites of chronic inflammation .
    Eg - Antrum
         - Junction of antral and body- fundic mucosa (division
    between the inflamed antral mucosa and normal acid secreting
     Pangastritis - When there is extensive gastritis, the ulcers are
    more proximally situated. In elderly patients gastric ulcers are
    more proximally situated as there is proximal migration of the
    antral-body mucosal junction.
    Other factors causing peptic ulcer:

     Peptic ulcer caused due to high gastrin level and excess acid
     production. Gastrinoma may cause multiple peptic ulceration
     as in Zollinger Ellison syndrome. There is increased parietal
     cell mass.

     Peptic ulcers caused due to impaired mucosal defense . The
     gastric acid and pepsin levels are normal and no H.pylori are
    Chronic use of NSAIDs (aspirin) causes suppression of
     mucosal prostaglandin and direct irritative topical effect.
    Repeated use of corticosteroid in high dose.
    Cigarette smoking impair healing and favour recurrences.
    Alcoholic cirrhosis.
    Personality, psychological stress, ischemia.
Gross features:
  Gastric ulcers are usually single well delineated lesion.
 Shape: Round, oval or linear.

 Size: Usually less than 2cm in diameter.

Lesions less than 0.3 cm are likely to be shallow erosions.
Giant ulcers are usually greater than 3cm in diameter.
May also reach upto 10cm (particularly on lesser curvature ).
Mortality rate is higher in these patients.
Size does not differentiate benign from malignant ulcer.
Some carcinomatous ulcers are less than 4cm and 10%
of benign ulcers are more than 4cm .
Gross features:
 Usually level with the surrounding mucosa or slightly
 The proximal margin has a overhanging border and distal
  margin has a sloping border.
 Converging mucosal folds extend to its margin.
 Heaping up of of margin is rare in benign ulcer .
 Prominent marginal nodularity about the ulcer should
  suggest the presence of carcinoma .
 Fungal infection can also give a nodular appearance of
  the ulcer margin
Gross features:

Depth of penetration :
 Superficial ulcer penetrate the mucosa into the
  muscularis mucosae.
 Deeply excavated ulcers having their bases on the
  muscularis propria.
 Entire wall is penetrated and the ulcer base is adherant

   to the pancreas, omental fat or liver. Free perforation
  into peritoneal cavity may occur.
Gross features:
Base of ulcer:
 Smooth and clean (peptic digestion of any exudate).
 Thrombosed or patent blood vessels are evident at
the base.
Surrounding gastric mucosa:
 Puckering of surrounding mucosa. The mucosal fold
radiates from the crater in a spoke- like fashion.
 Edematous and reddened due to gastritis.
 Gastric wall:
 Scarring involve the entire thickness . Subserosal
 fibrosis and inflammation present.
 Regional lymphnodes are enlarged.
Biopsy of peptic ulcer:

   Biopsy is necessary to distinguish between benign and
    malignant ulcers.
    Biopsy should be taken from the ulcer edge, at least
    from each quadrant.
    Upto 10-12 biopsies may be taken to exclude cancer.
    Repeat endoscopy may be necessary if biopsies are
    negative and there is high index of suspicion.
Microscopic features

Four distinct layers are present in a peptic ulcer.
   Surface coat of purulent exudate, bacteria and necrotic
    Fibrinoid necrosis.
    Granulation tissue.
    Fibrosis replacing the muscle wall and extending into
    Microscopic features:
  Thickening of vessels caused by subendothelial fibrous
 Hypertrophy of nerve bundles.
 Mucosa surrounding the ulcer is pyloric type.
 Necrotic surface shows superimposed infection by candida
 In case of H. pylori infection following features are noted
at the ulcer edge : loss of apical portion of cells,
                    dropout of epithelial cells,
                    erosion, cellular tufts.
Microscopic features:

 Healing process-
    Regenerating epithelium grows over the over the surface,
     (any epithelium growing above an area where muscularis
     mucosa is interrupted is regarded as regenerating).
     Intestinal metaplasia
     May contain chief and parietal cells (ulcer in the fundus
     Gastritis remains after ulcer has healed. (D/D In erosive
     gastritis & stress ulcer, gastritis in adjacent mucosa is
     generally absent)

Cellular atypia may be present in ulcers caused by arterial
     infusion chemotherapy.
      Eradication of H.pylori (proton pump inhibitor in
      combination with antibiotics)
      Acid suppression- Antacid & or H2 blockers
      Cessation of NSAIDS.
  Criteria for reduction of the size of ulcer crater.
  Reduction of crater size by 50% over 6-8 weeks of
      intensive medical management.
   Subtotal gastric resection without vagotomy and
    drainage (gastroenterostomy or pyloroplasty)
   Truncal vagotomy plus antrectomy

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