Peptic Ulcer Pharmacology

  1. Three common causes of peptic ulcer disease:
    • H pylori
    • NSAID use
    • Stress related mucosal damage (stress ulcer)
  2. H pylori often leads to _____ ulcer, while NSAID induced is more often ____ ulcer
    • Duodenal
    • Stomach
  3. What are defensive factors that prevent PUD from developing?
    • Mucus
    • Bicarbonate
    • Blood flow
    • Prostaglandins
  4. What are aggressive factors that could lead to PUD?
    • H pylori
    • NSAIDs
    • Acid
    • Pepsin
    • Smoking
  5. True/false: Duodenal ulcer, pain is elicited usually after ingestion of food
    False; duodenal ulcer, pain is relieved by food.
  6. What’s the H pylori treatment regimen?
    • Two antibiotics + one antisecretory drug (PPI)
    • Or two antibiotics + one ant secretory drug and bismuth
  7. What are the antibiotics used to treat H pylori?
    • Clarithromycin
    • Amoxicillin
    • Metronidazole
    • Tetracycline
    • Bismuth (yes, pepto bismol has topical antibacterial effects apparently)
  8. True/false: Abx substitutions not recommended
    True
  9. True/false: H2 blockers could be used instead of PPIs
    True, but not necessarily recommended
  10. MOA of amoxicillin?
    Inhibits cell wall biosynthesis
  11. MOA of clarithromycin?
    Inhibits RNA-depended protein synthesis
  12. MOA of metronidazole?
    Inhibits nucleic acid synthesis
  13. MOA of Tetracycline?
    Inhibits protein synthesis
  14. Adverse effect of amoxicillin?
    Diarrhea, rash, allergic reaction
  15. Adverse effect of Clarithromycin?
    Diarrhea, N/v, taste changes, QT prolongation
  16. Adverse effect of Metronidazole?
    N/v, HA, taste changes
  17. Adverse effect of Tetracycline?
    Upset stomach, flatulence, tooth discoloration
  18. Adverse effect of bismuth subsalicylate?
    Blackened stools, blackened tongue
  19. Which abx used to treat H pylori could cause QT prolongation?
    Clarithromycin
  20. Which antibiotics should you reduced the dosage for if creatinine clearance is less than 30?
    • Amoxicillin
    • Clarithromycin
    • Tetracycline
    • (Gotta ACT when CrCl < 30 yo!)
  21. Drugs with -tidine stem is _______. Drugs with -prazole stem is _______
    • H2 receptor antagonist
    • PPI (Prazole = PPI)
  22. What is the MOA of PPI?
    Directly inhibit the H+/K+ ATPase on the apical membrane
  23. _____ has inhibitory effect on cAMP, which ultimately leads to decreased H+ secretion
    Prostaglandin
  24. What are adverse effects of PPI?
    • HA, Nausea, abd pain
    • Chronically, drug interactions, and could increase gastric pH overtime (yes, increase)
  25. True/false: PPIs inhibits CYP2Cp and CYP2C19
    True
  26. Which PPI has an immediate release when taken with sodium bicarb/ magnesium hydroxide?
    Omeprazole
  27. True/false: all PPI are formulated as immediate release
    False; they are all formulated as delayed release (enteric coated)
  28. True/false: H2 receptor antagonist are better used for bleeding ulcers
    False; PPIs are most likely superior for bleeding ulcers
  29. In bleeding ulcers, which drug (PPI/ H2RA) would you use?
    PPI
  30. What is the MOA of H2RA?
    Blocks the histamine receptor on the basolateral membrane, so histamine could not bind, and cAMP would therefore not be stimulated. Ultimately, decreased H+ secretion
  31. Adverse effects of H2RA?
    • HA, dizziness
    • Chronically, could potentially cause thrombocytopenia, and also could increase gastric pH over time
  32. What is the usual daily dose for PPI? H2RA?
    • Once a day for PPI
    • Twice daily for H2RA
  33. True/false: some H2RA have CYP interactions
    True
  34. True/false: H2RA and PPIs have equal efficacy for non-bleeding ulcers, stress ulcer prophylaxis
    True
  35. Which COX isoform produces protective prostaglandin, and plays the primary role in how NSAID could cause peptic ulcers?
    COX-1
  36. What is the treatment strategy for NSAID induced peptic ulcer?
    • discontinue NSIAD if possible and start PPI/H2RA / sucralfate
    • Or decrease dose of NSAID and start PPI/ H2RA/ sucralfate/ misoprostol
  37. What is the MOA of Misoprostol?
    • Prostaglandin receptor agonist.
    • Misoprostol is a synthetic analog of PGE 1
  38. When is Misoprostol used to treat ulcers?
    when it is NSAID induced, and you can’t completely discontinue NSAID, so you add misoprostol in treatment
  39. Which drug can form a complex of albumin/fibrinogen at ulcer site creating a protective barrier?
    sucralfate
  40. True/false: you have to take sucralfate on an empty stomach
    True
  41. True/false: misoprostol can increase PGE2
    False; Sucralfate increases PGE 2, misoprostol is an PGE 1 analog
  42. True/false: Misoprostol should be taken with food
    true
  43. When is misoprostol use contraindicated?
    in pregnancy because it stimulate uterine contractions
  44. What is stress related mucosal damage?
    acute erosive gastritis that occurs in response to physiologic stress, mostly in critically ill patients
  45. What are way that critical illness can lead to acute stress ulcer?
    • can lead to hypovolemia which leads to decreased cardiac output
    • increase proinflammatory cytokine release
    • Increased in catecholamines which leads to vasoconstriction
    • And all these leads to splanchnic hypoperfusion and ultimately leads to acute stress ulcer
  46. Which drugs are used to prevent SRMD?
    • PPIS
    • H2Ras
    • Antacids
    • Prokinetic agents
  47. True/false: Antacids are usually used for PUD
    False; antacids like TUMS are not usually used for PUD, they are more often used for episodic heartburn
  48. What is an alumni based antacid?
    Mylanta
  49. What is a magnesium based antacid?
    • Maalox
    • Milk of magnesia
  50. What is calcium based antacid?
    Calcium carbonate (tums)
  51. True/false: pepto bismol is an antacid
    True; but remember it can also have some antibacterial effects
  52. What are adverse effects of antacids?
    • Flatulence, diarrhea.
    • Aluminum: constipation
    • Magnesium: diarrhea
  53. What are prokinetic agents?
    • Azithromycin
    • Cisapride
    • Metoclopramide
    • Bethanechol
  54. What is the MOA of prokinetic agents?
    Increase gastric emptying
  55. Which prokinetic agent agonizes motilin receptors?
    Azithromycin
  56. Which prokinetic agent works by increasing Ach?
    • Cisapride
    • Metoclopramide
  57. Which prokinetic agent works by directly stimulating muscarinic receptors?
    Bethanechol
  58. Which prokinetic agent should not be used due to QT prolongation/ Torsades
    Cisapride
  59. Which prokinetic agent blocks dopamine and 5HT2 receptors?
    metoclopramide
Author
lykthrnn
ID
346854
Card Set
Peptic Ulcer Pharmacology
Description
GI Midterm- Pharmacology
Updated