PUD Flashcards

(1 cards)

1
Q

Diagnosis
Pathology on chest x ray
Risk factors leading to perforation
How nsaids can cause peptic ulceration
How to manage
Mechanism of PPI
Actions of HCL
Phases of gastric acid secretion

A

• NSAID’s
• H. pylori
• Steroids
• Previous peptic ulcers
• Malignancy

Topical irritant effect of these drugs on the epithelium,
• Impairment of the barrier properties of the mucosa
• Suppression of gastric prostaglandin synthesis, (inhibition of cyclooxygenase)
• Reduction of gastric mucosal blood flow
• Interference with the repair of superficial injury.

  1. Initial resuscitation (always first):
    • ABC, IV access, fluids, NG tube, urinary catheter, IV antibiotics, PPI.
  2. Surgical options:
    • Omental patch repair (Graham’s patch):
    • Standard emergency procedure.
    • Suture perforation with omental patch, peritoneal lavage, place drain..
  3. For gastric ulcer perforation:
    • Same approach (patch repair, lavage, drain).
    • But add biopsy of ulcer edge to exclude malignancy.

e PPI binds irreversibly to a hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal cells and blocks the secretion of hydrogen ions, which combine with chloride ions in the stomach lumen to form HCL

• Activates pepsinogen to pepsin which help in proteolysis
• Antimicrobial
• Stimulates small intestinal mucosa to release CCK and secretin
• Promotes absorption of calcium and iron in the small intestine

  1. Cephalic phase (smell / taste of food)
    • 30% acid produced
    • Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
  2. Gastric phase (distension of stomach)
    • 60% acid produced
    • Stomach distension / low H + / peptides causes Gastrin release
  3. Intestinal phase (food in duodenum)
    • 10% acid produced
    • High acidity / distension / hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes.
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