PEPTIC ULCER

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PEPTIC ULCER
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• 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.

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DEFINITION

• Imbalance between aggressive protective factors

• Aggressive factors
• Gastric acid
• Proteolytic enzyme
• Protective factors
• Mucosal layer
• Bicarbonate secretion
• Prostaglandins

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Gastric physiologyAcid secretion

• The human stomach contains about 1 billion
  parietal cells
• These are located in the walls of the
  midsection of the oxyntic glands
• Oxyntic glands are the secretory glands of the
  gastric mucosa
• Oxyntic glands also contin chief, mucous,
  endocrine, and somatostatin cells

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• There are three primary pathways that stimulate
  gastric acid secretion
• 1) The neurocrine pathway which delivers
  transmitters such as acetylcholine
  post-ganglionic nerves on the stomach wall
• 2) The endocrine pathway which releases hormones
  such as gastrin
• 3) The paracrine pathway which releases histamine
  
• These pathways are interdependent
• Once pH is lt3.5, pepsinogen is converted to the
  active proteolytic enzyme pepsin

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• Pathogenesis of peptic ulcer
• 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 agents.

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Imbalance (Aggressive/Defensive Factors)

• Aggressive Factors
• H. pylori
• Acid Secretion
• Pepsinogen Secretion
• NSAIDS
• Cigarette smoking
• Corticosteroid use

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• Defensive Factors
• Mucus Production
• Bicarbonate Production
• Mucosal blood flow - more important in the
  development of stress ulcer
• High epithelial cell turnover
• Prostaglandins (PGE2) - stimulate mucus and
  bicarbonate production, and blood flow

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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. Pyrosis
• Pain worse at night and 1 to 3 hours after meal.
• Nausea, vomiting, bloating , belching and weight
  loss occur.
• Complication Anaemia, hemorrhage, perforation,
  obstruction. Malignant formation is rare and
  related to underlying gastritis.

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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 common).
• 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 Meckels diverticulum
  that contains ectopic gastric mucosa.

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H.Pylori
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Role of H. Pylori infection in the pathogenesis
of peptic ulcer

• 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.
• Mechanism
• 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.

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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 mucosa).
• 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.

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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 present.
• 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.

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Diagnostic Test and Procedures

• a) Routine
• Routine lab tests are not useful in
  establishing the diagnosis of uncomplicated PUD
• Hct, HgB, and stool hemoccult are useful to
  detect bleeding
• b) H.pylori test
• Histology
• Culture
• Biopsy/gram stain
• Biopsy/CLO test
• Urea breath test
• Serology

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Diagnosis

• Breath Test Carbon 14 Urea Test (see picture)
• Blood Test
• Endoscopy

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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
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• of benign ulcers are more than 4cm .

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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.

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Endoscopy
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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.

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Microscopic features

• Four distinct layers are present in a peptic
  ulcer.
• Surface coat of purulent exudate, bacteria and
  necrotic debris.
• Fibrinoid necrosis.
• Granulation tissue.
• Fibrosis replacing the muscle wall and extending
  into subserosa.

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Management

• MEDICAL TREATMENT
• a) Antisceretory/Anti-acid Agents
• 1) H2-blockers
• 2) Proton-pump inhibitors
• 3) Antacids
• b) Cytoprotectives
• 1) Misoprostil
• 2) Sucralfate
• c) H. pylori Agents

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• Eradication of H.pylori (proton pump inhibitor in
  combination with antibiotics)
• 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.
• Endoscopic
• SURGICAL TREATMENT

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Differentials

• Mesenteric ischemia
• Angina pectoris
• Biliary colic
• Pancreatitis

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Complication

• Hemorrhage
• Perforation
• Penetration
• Obstruction
• Malignancy

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