Peptic Ulcer Disease (PUD)

  •          Ulcer:
  •  – 5 mm or larger break in the lining of mucosa with appreciable depth at endoscopy or with evidence of     submucosal extension
  •             Erosion:
  •  – Mucosal break <5 mm
  •                PUD:
  • – Ulceration or erosion in the stomach, duodenum from a number of causes

               *More than half of PUD are asymptomatic

  •                 NSAID induced PUD:
  •   –  NSAID damage mucosa by inhibiting prostaglandin synthesis
  •  –  COX-1 inhibition reduces prostaglandin synthesis, which leads to reduction in mucosal defence
  •  –  Among patients who are about to start NSAID therapy, eradication of Hp reduces the subsequent risk of ulcer development
  •  –  Hp infection increases the risk of PUD in patients receiving low dose (<160mg) aspirin also
  •   –  15-30% patients receiving NSAID develop PUD
  •         Idiopathic and other causes of PUD (Non Hp, Non NSAID PUD)
  •                                 – Cocaine
  •                                  – Methamphetamine
  •                                  – Bisphosphonate
  •                                  – Glucocorticoid
  •                                  – Smoking
  •                                  – Stress
  •                                  – Type A personality
  •                                  – Excessive alcohol
  •                                  – Zollinger-ellison syndrome (ZES)
  •                                  – Systemic mastocytosis
  •                                  – Gastric cancer, lymphoma, crohn’s disease
  •                                 – Rare causes: eosinophilic gastroenteritis, viral infection
  •                                      
  •                                        Gastric Ulcer
  • – Most benign ulcers are found in antrum and lesser curvature at the junction of body and antrum
  • – GU often occur later in life,usually 55-70 years with peak in 6th decade
  • – GU patients have normal/decreased acid secretion
  • – Few patients with GU+DU have increased acid secretion
  • – 5% GU are malignant
  • – To exclude malignancy, a biopsy taken from the ulcer or perform Follow up endoscopy 12 weeks after starting acid suppressive medication to document complete healing
  • – Ulcer is more likely to be malignant if
  •        > Ulcer>3 cm
  •        > Association with mass

 

 

  • Diagnostic endoscopy in PUD
  •                      In case of GU in patients >40 years
  • – At least 6 biopsy of ulcer and surrounding folds should be taken
  • – If adequate biopsy is not feasible: Brushing and irrigation cytology should be obtained
  • – Biopsy should be deferred in acute bleeding of GU
  • – Ulcer biopsy in the setting of portal hypertensive gastropathy is controversial
  • – If biopsy is benign, EGD is repeated 8 weeks later to confirm healing of the GU
  • – 4% of apparently benign GU at initial endoscopy are subsequently found to be malignant

 

  •                                         Treatment of Hp Ulcer   
  •  – 10-14 day course of Hp eradication therapy is sufficient to heal DU and additional anti-secretory therapy is usually not required
  •  –  Follow up endoscopy to document ulcer healing is not recommended in DU. But UBT/Fecal antigen should be done to confirm Hp eradication
  • *Anti-secretory therapy after 7-10 day course of Hp eradication in case of GU is controversial.
  • *Follow up endoscopy is recommended in patients with large or complicated GU to document healing, exclude malignancy and confirm successful Hp eradication

 

  •   Treatment of NSAID induced ulcer
  • – Aspirin/NSAID should be discontinued if possible
  • – If discontinuation is possible: PPI/H₂RA heal ulcer
  • – If discontinuation is not possible: Continue PPI (PPI is more effective than H₂RA in this case)
  •  – Test for Hp and treat if possible

 

  • Treatment of Idiopathic ulcer/ other causes of ulcer
  •            – Long term maintenance therapy with PPI
  •           – Treatment of underlying disorder (e.g ZES)
  • Complications of PUD
  • GI hemorrhage
  •           *15% PUD bleeds
  •          *Bleeding and mortality rate is increased in patients >60 years age
  •          * Presents with hematemesis, coffee ground emesis, melena and rarely hemayochezia
  • – GI perforation 7%
  •               • NSAID induced ulcer perforation may have no H/O abdominal pain
  •               • Gastric outlet obstruction-2%

 

                                                  PUD BLEEDING                      

  • – Bleeding may be the first sign of an ulcer in 10-15% of clinically recognized cases
  • – 90% of clinically significant ulcer bleeds stop spontaneously
  • – Maintenance of anti-ulcer therapy traditionally has been given to all patients with a H/O bleeding ulcer
  • – Hp eradication reduces rebleeding rate

 

  •    Specific therapy of PUD bleeding
  • 1.Endoscopic therapy
  • – Injection method: Epinephrine
  • – Thermal therapy
  •         Contact: Heater probe, Bipolar probe
  •         Non-contact: Plasma coagulation, LASER
  • – Mechanical method: hemoclip
  • – Combination method
  •   2.Anti-secretory therapy: Continuous twice daily PPI for 72 hour (it prevents rebleeding)
  •    3.Surgical therapy:If failure to control massive bleeding after initial control
  •    4.Angiographic therapy: If patient is poor risk for surgery

 

 


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