1. What are the classic symptoms of GERD?
    • heartburn (pyrosis)
    • hypersalivation (water brash)
    • belching
    • regurgitation
    • acid taste in mouth
    • nausea
  2. What are the atypical symptoms of GERD? How do we evaluate and treat?
    • Nonallergic asthma
    • chronic cough
    • hoarseness
    • pharyngitis
    • chest pain
    • dental erosions

    if pt has chronic cough, ambulatory reflux monitoring is preferred approach for evaluation

    if pt has non-cardiac chest pain use 20mg omeprazole BID for 1-8 weeks
  3. What are the Alarm Symptoms of GERD? Which pts need to be referred for endoscopy?
    • continual pain
    • dysphagia
    • odynophagia (pain on swallowing)
    • unexplained weight loss
    • choking
    • bleeding

    if pt has alarm symptoms, is >45 yo, is refractory to treatment, they should be referred for endoscopy
  4. What foods lower esophageal sphincter pressure?
    • peppermint
    • spearmint
    • chocolate
    • coffee, cola, tea
    • garlic
    • onion
    • fatty meals
    • chili peppers
  5. What are 3 main drugs that lower esophogeal sphincter pressure?
    • beta blockers
    • calcium channel blockers
    • nicotine
  6. name some meds and foods that can couse esophageal injury
    • NSAIDs, ASA, bisphosphonates, iron salts
    • acidic foods, alcohol, spicy foods, coffee
  7. How long should a patient have tried lifestyle changes with no relief before instituting acid suppression therapy?
    2 weeks
  8. What is "step-down" treatment for GERD? When should it be used?
    • start with high dose QD to BID PPI then step down to a lower PPI dose, then to an H2RA, then taper off
    • used for severe disease
  9. What is "step-up" treatment for GERD?
    • traditional treatment
    • first initiate lifestyle changes, progress to H2RAs, then to PPIs, then to surgery
  10. What is the mainstay of treatment for GERD?
    acid suppression
  11. what are options for appropriate initial treatment for GERD?
    • antacids
    • OTC acid suppressive agents
  12. Which GERD meds provide rapid relief and healing of esophagitis in the highest percentage of patients?
  13. Name 4 types of antacids
    • sodium bicarbonate
    • calcium carbonate (tums, maalox)
    • magnesium salts (mylanta)
    • aluminum salts (maalox, mylanta)
  14. Which type of antacid may exacerbate HTN and CHF?
    sodium bicarbonate
  15. Which type of antacids cause constipation? Diarrhea?
    • Constipation: calcium carbonate, aluminum salts
    • Diarrhea: magnesium salts
  16. Which type of antacid should be avoided in renal failure?
    magnesium salts
  17. Which type of antacids might be a good choice in a chronic kidney disease patient and why?
    aluminum salts because they help to absorb excess phosphate
  18. MOA of antacids
    • neutralize acid and increase gastric pH
    • also decrease pepsin and gastrin
    • increase LES pressure
  19. What is alginic acid?
    • an "inactive" ingredient in many antacids
    • it forms a protective barrier between the esophagus and gastric contents
  20. Antacids place in therapy
    • 1st line for intermittent sx or as breakthrough for PPI/H2RA therapy
    • give immediate symptom relief
  21. DIs with antacids
    • chelation with FQs, TCs
    • reduced abs d/t pH increases with ketoconazole, itraconazole, iron
  22. name 4 H2 receptor antagonists
    • cimetidine (tagamet)
    • famotidine (pepcid)
    • ranitidine (zantac)
    • nizatidine (axid)
  23. MOA of H2RAs
    competitive (reversible) inhibition of H2 receptors on parietal cell - decrease gastric secretion
  24. What do we use low dose H2RAs for?
    treatment of mild symptomatic GERD
  25. What do we use standard dose H2RAs for?
    treatment of mild-moderate GERD (BID dosing)
  26. What do we use high doses of H2RAs for?
    to heal erosive esophagitis (QID dosing)
  27. H2RAs place in therapy
    • on-demand therapy for intermittent mild-to-moderate GERD sx
    • preventive dosing before meals or exercise
    • high doses (Rx) are for severe sx or maintenance therapy
  28. Duration of therapy with H2RAs
    8 weeks +
  29. How soon do antisecretory effects begin with H2RAs? How long do they last?
    • begin w/in 1 hr
    • last 6-12 hr
  30. AEs of H2RAs
    • CNS effects - elderly at increased risk
    • Hematologic effects - rare - (decr platelets and WBCs - monitor CBC)
    • N/V/D/ constipation
    • Endocrine - cimetidine assoc with gynecomastia (rare - with prolonged use)
  31. Renal dosage adjustments for standard doses of H2RAs
    • Ranitidine: if CrCl < 50, give 150 mg qd
    • Famotidine: if CrCl < 50, give 20 mg qd
    • Cimetidine: if CrCl < 30, give 300 mg q12h
    • Nizatidine: if CrCl 20-50, give 150 mg qd. If < 20, give 150 mg QOD
  32. DIs with H2RAs
    • affect absorption of ketoconazole, itraconazole, iron
    • cimetidine inhibits lots of CYP enzymes (affects warfarin, phenytoin, diazepam, theophylline). Use famotidine or ranitidine instead
  33. Can tolerance develop with H2RAs?
  34. Name 6 proton pump inhibitors
    • omeprazole (prilosec)
    • lansoprazole (prevacid)
    • esomeprazole (nexium)
    • pantoprazole (protonix)
    • rabeprazole (aciphex)
    • dexlansoprazole (kapidex)
  35. What are the equivalent doses for GERD of the PPIs?
    • omeprazole 20 mg
    • esomeprazole 20 mg
    • rabeprazole 20 mg
    • lansoprazole 30 mg
    • pantoprazole 40 mg
    • dexlansoprazole 60 mg
  36. MOA of PPIs
    irreversibly inhibit H+/K+/ATPase - final step in gastric secretion
  37. preferred treatment in pt with esophagitis
  38. Do H2RAs or PPIs have a longer DOA?
    PPIs typically do
  39. PPIs place in therapy
    most effective tx for short-term and long-term mgmt of GERD and erosive disease
  40. When should PPIs be taken?
    30 minutes prior to a meal
  41. How long does it take to get symptom relief and complete relief with PPIs? Why?
    • 2-4 h for symptom relief
    • 3-5 d for complet relief
    • because PPIs only inhibit active proton pumps
  42. Duration of therapy with PPIs
    4-8 weeks (possibly longer)
  43. DIs with PPIs
    • drugs with pH dependent absorption (ketoconazole, itraconazole)
    • Omeprazole inhibits 2C19 so can affect warfarin (decr. PT)
    • Clopidogrel - is efficacy is decr. with omeprazole. CLINICALLY SIGNIFICANT. If possible use H2RA instead, or pantoprazole or esomeprazole.
  44. For healing GERD-related esophagitis which PPI is best?
    none - they are equal
  45. Options for optimizing therapy in patients refractive to PPIs
    • increase dosing frequency
    • increase dose
    • add a 2nd drug (hs dose of H2RA, prokinetic)
    • switch to different PPI
    • for nocturnal sx, may add H2RA
    • anti-reflux surgery - last line
  46. Name 3 promotility agents
    • metoclopramide
    • bethanechol
    • cisapride
  47. What is the MOA of promotility agents?
    facilitate increased gastric emptying
  48. Promotility agents place in therapy
    adjunctive therapy for GERD - used in combo with H2RAs in pts with motility probs and in pts who fail high dose PPIs
  49. Why are promotility agents not routinely used?
    • the risks outweigh the benefits
    • they have lots of SEs
    • require multiple daily doses
  50. Metoclopramide MOA, AEs and CIs
    • promotility agent - dopamine antagonist
    • increases LES tone and accelerates gastric emptying
    • dosed up to QID
    • AEs - dizziness, fatigue, somnolence, drowsiness, EPS, hyperprolactinemia
    • CI'd - Parkinsons, mechanical obstruction, other dopamine antagonists or anticholinergics, pheochromocytoma
  51. Bethanechol MOA, AEs
    • promotility agent - cholinergic agonist
    • AEs - diarrhea, blurred vision, abdominal cramping
    • May increase gastric production
  52. Cisapride MOA, Efficacy, AEs
    • promotility agent
    • efficacy similar to H2RAs
    • available on restricted basis only
    • AEs - QT prolongation and cardiac arrhythmias when in combo with 3A4 inhibitors
  53. name a mucosal protectant for GERD
  54. MOA, place in therapy and AEs of sucralfate
    • Dosed QID 30 min prior to meal
    • MOA - nonabsorbable aluminum salt - coats stomach
    • Place in therapy - not often used in GERD
    • AEs - lots of chelation DIs, accumulation of aluminum in renal failure
  55. What is fundoplication?
    • anti-reflux surgery
    • last line therapy for GERD
    • pts still can't d/c meds
  56. When to use GERD maintenance therapy
    • if sx return w/in 3 months of tapering off meds
    • if pt has complications (Barretts esophagus, strictures, hemorrhage)
  57. Treatment options for GERD maintenance therapy
    • H2RA (for mild disease) - only ranitidine 150 mg BID is approved for maintenance of healing erosive esophagitis
    • PPI (for moderate to severe esophagitis)
    • "on-demand" PPI for endoscopy-negative GERD
  58. Recommended treatment regimen for pt with intermittent mild heartburn
    lifestyle modifications + antacids AND/OR OTC low-dose H2RA (up to BID) OR OTC PPI (QD)
  59. Recommended treatment regimen for symptomatic relief of GERD (mild-to-moderate typical symptoms or atypical symptoms with non-erosive GERD)
    lifestyle modifications + rx-strength acid suppression therapy (H2RA for 6-12 weeks OR PPI for 4-8 weeks)
  60. Recommended treatment regimen for healing of erosive esophagitis or treatment of pts presenting with moderate to severe symptoms or complications
    lifestyle modifications + PPIs for 4-16 weeks up to BID OR high-dose H2RAs for 8-12 weeks
  61. What are the 2 classifications of peptic ulcer disease?
    • duodenal ulcer
    • gastric ulcer
  62. What are the causes of duodenal ulcers? Gastric ulcers?
    • Duodenal: H. pylori infx (95%), NSAIDs (less common - Zollinger-Ellison syndrome, hypercalcemia, neoplasia, CMV, herpes)
    • Gastric: H. pylori infx, NSAIDs, stress (less common - Crohn's, CMV, herpes)
  63. Signs & symptoms of duodenal and gastric ulcers
    • Both: epigastric pain, heartburn, belching, bloated feeling, nausea, anorexia, GI bleeding/hematemesis
    • Duodenal: worse at night and the pain occurs 1-3 hours post meal. Relieved by eating.
    • Gastric: pain is worse with eating.
  64. Duration of acute treatment for ulcers
    • uncomplicated duodenal ulcer 4+ weeks
    • uncomplicated gastric ulcer 6+ weeks
  65. risk factors for NSAID induced ulcer
    • Age > 60 years
    • increased NSAID dose
    • longer duration of treatment
    • intrinsic NSAID toxicity
    • hx of PUD
    • concurrent use of corticosteroids or anticoagulants
    • underlying CV or rheumatologic disease
    • use of multiple NSAIDs
  66. What is H. pylori?
    • G (-) bacteria found between gastric epithelial cells and the mucus layer
    • it increases ulceration and damage
    • can lead to gastric cancer
  67. Which patients is H. pylori testing indicated for?
    • active ulcer disease
    • history of PUD
    • MALT lymphoma
  68. When would we use triple therapy for treatment of H. pylori ulcers? What is triple therapy?
    • Only if it is known to be susceptible to the agents
    • Triple therapy is one antisecretory agent (PPI preferred) + 2 antibiotics
  69. What is the preferred duration of therapy for treatment of H.pylori ulcers?
    10-14 d
  70. When should quadruple-based therapy be used for treatment of H. pylori ulcers? How long should it be used?
    • Use if initial tx fails or if there's resistance
    • Use for 14 days
  71. What do we need to consider when choosing therapy for H. pylori ulcers?
    • Efficacy (should be > 90% and >85% in resistant strains)
    • Tolerability
    • DIs
    • Antibiotic resistance
    • cost
    • compliance (many multiple daily doses needed)
  72. What effect do salicylates have on the feces?
    they make it turn dark in color
  73. What is the bismuth quadruple treatment regimen for H. pylori?
    • bismuth subsalicylate 525 QID + metronidazole 500 mg TID + tetracycline 500 mg QID + PPI (or ulcer-healing dose of H2RA for 4-6 weeks)
    • Duration is 14 days
    • can substitute Amoxicillin 500 mg or Clarithromycin 250-500 mg QID for the TC
  74. What is concomitant therapy for H. pylori?
    Amox, clarithromycin, and metronidazole (or tinidazole) + PPI for 10 - 14 d
  75. What is sequential therapy for H.pylori?
    • Amox + PPI BID x 5 days
    • then clarithromycin + metronidazole + PPI BID for 5 more days
  76. What is sequential-concomitant therapy for H. pylori?
    • Amox + PPI BID x 7 d
    • then Amox, Clarith, and metronidazole for 7 more days
  77. How do NSAIDs cause ulcers?
    • cause direct or topical damage
    • inhibit prostaglandins
  78. Name the partially selective NSAIDs
    • etodolac
    • meloxicam
    • diclofenac
    • celecoxib
    • nabumetone
  79. What is the DOC for healing and secondary prevention of NSAID induced ulcers? What is the duration of treatment?
    PPI for 4 weeks (would need maintenance therapy if pt continued on NSAID)
  80. What are the standard doses of PPIs for PUD?
    • omeprazole 20-40mg qd
    • esomeprazole 20-40mg qd
    • rabeprazole 20 mg qd
    • lansoprazole 15-30 mg qd
    • pantoprazole 40 mg qd
    • dexlansoprazole 30-60 mg qd
    • sucralfate 1 g qid or 2 g bid
  81. What prostaglandin is used for NSAID induced ulcers? What are its advantages, disadvantages and CIs?
    • misoprostol
    • (+) as effective as PPI for healing/secondary prevention
    • (-) MDD, dose dependent AEs - diarrhea, abd pain, nausea, flatulence
    • CI - pregnancy Category X d/t bleeding/spontaneous abortion
  82. Are H2RAs useful in preventing ulcers?
    • inferior in healing and preventing recurrence of gastric ulcers
    • standard dose can prevent NSAID induced duodenal ulcers
  83. When is an ulcer considered refractory?
    when symptoms, or the ulcer, or both persist for > 8 weeks for duodenal or > 12 weeks for gastric despite treatment
  84. How are refractory ulcers treated?
    • Higher PPI
    • Maintenance treatment with healing dose of PPI may be needed
    • No benefit in switching between different H2RAs or PPIs
    • Concurrent PPIs and H2RAs no benefit
    • Combo with misoprostol or sucralfate no benefit
    • May need surgery
  85. Define Zollinger-Ellison Syndrome (ZES)
    hypergastric secretion with recurrent peptic ulcerations resulting from a gastrin producing tumor (gastrinoma)
  86. Symptoms of ZES
    • recurrent peptic ulcers
    • heartburn
    • diarrhea
  87. What is used for treatment of ZES?
    • PPIs are first line (H2RAs don't work well enough)
    • High doses (e.g. 60 mg omeprazole)
    • Long term
    • May use octreotide to directly inhibit acid secretion. 100-250 mcg SQ TID
    • May require surgery or chemotherapy
  88. Causes of upper GI bleed
    • PUD
    • esophagitis
    • erosive disease
    • esophageal varices
    • stress ulcers
  89. Sx of upper GI bleed
    • hematemesis (coffee-ground)
    • N/V/D, melena
    • Hypotension and assoc organ dysfxn (renal/hepatic/cardiac/cerebral hypoperfusion)
    • Sx of blood loss anemia (fatigue, low Hgb/Hct)
  90. How is upper GI bleeding treated?
    • Endoscopy w/in 24 h and ablation if needed
    • Remove meds contributing to bleeding
    • High dose PPIs (bolus then infusion - can use oral)
    • Use of H2RAs or octreotide not recommended
  91. Indications for IV PPIs
    • pts with GERD or ZES and no enteral access
    • acute GI bleed
    • Prophylaxis of stress ulcers and clinically important bleeding
    • prevention of rebleeding from PUD
    • induction of anesthesia
  92. Define stress ulcer
    acute superficial inflammatory lesions of the gastric mucosa induced when an individual is subjected to abnormally elevated physiological demands
  93. Stress vs. Non-stress ulcers
    • Stress: multiple, acute, asymptomatic, acid/pepsin secretory mucosa
    • Non-stress: usually solitary, chronic inflammation, symptomatic (pain, burning, discomfort), distal stomach/duodenum (e.g. regular PUD ulcers)
  94. What is the pathogenesis of stress ulcers?
    • hypoperfusion of GIT - decreases protective mucosal mechanisms
    • altered susceptibility to gastric acid
    • loss of defense mechanisms (mucous/bicarb layer, prostaglandins, cellular renewal)
  95. What are the 3 main independent risk factors for stress ulcer bleeding?
    • Mechanical ventilation > 48 hours
    • Coagulopathy (platelets < 50,000; INR > 1.5)
    • GI bleeding/ulceration within past year
  96. Pharmacologic prevention of stress ulcers
    • Antacids
    • H2RAs
    • PPIs
    • Sucralfate
  97. Which meds are first line therapy for prevention of stress ulcers? What are some advantages and disadvantages?
    • H2RAs
    • (+) good efficacy data, inexpensive, easy to add to TPN, available PO and IV
    • (-) must dose adjust in renal impairment, higher pH may increase risk of bacterial colonization
  98. Dosing of Famotidine and Ranitidine in stress ulcer prophylaxis for normal and reduced renal function
    Famotidine: normal renal fxn 20 mg BID PO, NG, IV; if CrCl < 30, give 20 mg QD PO, NG, IV

    Ranitidine: normal renal fxn 150 mg BID PO or NG, 50 mg q6-8h IV; if CrCl < 50, give 150 mg QD or BID PO or NG or 50 mg q12-24h IV
  99. Guidelines for stress ulcer prophylaxis
    • No specific guidelines
    • H2RAs are 1st line (pt on vent, INR > 1.5, Hx GI bleed)
    • PPIs are 2nd or 3rd line
    • Sucralfate is 2nd or 3rd line
  100. When should stress ulcer prophylaxis be d/c?
    • when pt is transferred out of ICU
    • if pt in ICU has < 2 risk factors
    • may need to continue PPI or H2RA if pt has other disease states (GERD, PUD, high-dose steroids)
Card Set
524 Exam 6 Dr. Elder GERD, etc.