Peptic Ulcer Disease (PUD)

PUD (GU, DU, NUD (non ulcer dyspepsia))

  • Disruption of normal mucosal defense & healing mechanisms
  • Aggressive factors (gastric acid, pepsin)
  • Defensive factors (mucus, bicarb, PGs)
  • Generally diagnose by testing hematocrit, hemoglobin, hemoccult stool (in order to detect bleeding)
  • NSAIDs are the most important risk factor of GI bleeds & perforations
    • DU more likely to bleed than GU but GU bleeds have a higher mortality rate
    • After d/c NSAIDs, use PPIs for 2-4 weeks (DU) or 4-8 weeks (GU);  uses APAP or less damaging NSAID
    • Perforation are also more likely to cause death in patients with GUs than DUs.  High incidence of Hp ulcers w/ perforations.
      • Presents as a sudden, sharp pain
    • NSAIDs cause direct topical irritation of the gastric epithelium but they also systemically inhibit PG synthesis
    • NSAIDs inhibit COX   (inhibiting COX-1–results in adverse effects to stomach, kidney, intestine, etc)  (inhibiting COX-2–inhibits inflammation)
      • COX-2 selective (less GI effects, but CV effects):  celecoxib (celebrex), meloxicam (mobic)
  • Gastric outlet obstruction:  not common, but caused by scarring, edema or a blocking of the pyloric channel
    • Symptoms:  N/V, anorexia, weight loss, bloating, early satiety
    • Usually occurs in patients w/ chronic PUD

Differentiation between various types of gastric disorders

  • Silent ulcer–NSAID induced ulcers (common in elderly)
    • Elderly don’t feel as much pain
  • NUD–ulcer-like symptoms in the absence of peptic ulceration
  • DU –food may relieve pain**, nocturnal pain, pain between meals, episodic
  • GU–food may precipitate or accentuate pain, N/V, anorexia (weight loss)

Risk factors for the development of peptic ulcer disease (PUD)

  • Past history of PUD, Upper GI bleeds, NSAID related GI effects
  • Use of corticosteroids or anticoagulants with NSAIDs
  • Increased age, Smoking, alcohol, stress

PUD treatment:

  • Goals:  relieve pain, heal ulcer, prevent reoccurrence, reduce complications
  • Lifestyle modifications:  reduce stress, quit smoking, avoid food/beverages (EtOH), stop NSAIDs, eradicate Hp if present (biaxin, clarithomycin)
  • Meds: antacids, H2RAs (pepcid), PPIs, sucralfate, bismuth
    • Antacids (Mg/Al)–admin after meals, neutralize acid for 2-3 hours
      • Separate from tetracyclines, warfarin, etc by 2 hours (b/c of chelation)
    • H2RAs–Ranitidine (zantac), famotidine (pepcid), bizantidine (axid), cimetidine (tagamet)
      • Used for treatment & maintenance of DU & GU (higher dose needed for GU)
    • PPIs–omeprazole (prilosec), lansoprazole (prevacid)–iv, rabeprazole (aciphex), pantoprazole (protonix)–iv, esomeprazole (nexium)–iv
      • May mix capsules w/ apple sauce/apple juice
      • Zegerid = bicarb + omeprazole
    • Sucralfate (Al)–provides protective cover/bandage over ulcer for up to 6 hours
      • Requires acidic environment (don’t use in combo w/ PPIs)
      • Minimal systemic absorption; inhibits pepsin; adsorbs bile salts; stimulates PGs, doesn’t affect gastric acid secretion
    • Bismuth–Pepto-bismol, maalox, kaopectate
      • Doesn’t inhibit or neutralize acid
  • Refractory ulcers: take care of causes, use a higher PPI dose, don’t switch agents in the same category, no benefit of combining H2RAs & PPIs
  • Helicobacter pylori:  causes histological gastritis.  Risk factor for PUD, gastric adenocarcinoma, MALT lymphoma
    • Not related to gender/smoking/NSAIDs
    • Diagnose:  antibody testing, urease test, urea breath test, gastric biopsy, culture
    • Treatment:  2 or 3 antibiotics + an antisecretory agent
      • 10-14 days
    • Triple therapy:  PPI + clarithomycin + amoxicillin (or metronidazole)
    • Quadruple therapy (preferred):  bismuth subsalicylate + tetracycline + metronidazole + PPI (or H2RA)
      • Bismuth subsalicylate+ tetracycline + metronidazole + PPI
      • Sequential therapy: PPI + amoxicillin x 5 days
        • Followed by PPI + clarithromycin + metronidazole x 5 days
  • Treatment in patients who are going to need to continue to take an NSAID:
    • Give w/ food +/- antacids                (higher doses of PPIs w/ GU than DU)

Conventional Dose for Gastric Ulcer (GU)

Conventional Dose for Duodenal Ulcer (DU)

Omeprazole (Prilosec)

40 mg PO QD

20 mg PO QD

Lansoprazole (Prevacid)

30 mg PO QD

15 mg PO QD

Rabeprazole (Aciphex)*

20 mg PO QD

20 mg PO QD

Pantoprazole (Protonix)

40 mg PO QD

40 mg PO QD

  • PPI’s significantly reduce ulcer formation in patients taking NSAIDs or COX-II inhibitors
  • NO H2RAs, sulcrafate
  • Prevention for NSAID induced ulcers:
    • Misoprostolol:  increases PGs, dosage: 200mcg BID-QID, contraindicated in pregos.  Sometimes used in combo w/ diclofenac (NSAID) to increase compliance
  • Zollinger-ellison syndrome (uncommon):  Gastrinoma– gastrin producing tumor that causes gastric acid hypersecretion
    • Presents as severe, recurrent peptic ulceration (epigastric pain, esophagitis, GI bleeds, perforation) most often in the duodenum
    • SE: diarrhea, steatorrhea (fat in stool)
    • Vitamin B12 malabsorption
    • Treatment:
      • omeprazole/lansoprazole/rabeprazole–60mg/day
        • Admin q 8-12 hours
      • Octreotide (sandostatin)–100-250mcg subcutaneously TID

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