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Pharmacology-PA

GI Lecture #1

QuestionAnswer
1. What are the factors influencing PUD? Hydrochloric acid, pepsin, Alcohol, nicotine, Gastric mucosal ischemia, Helicobacter pylori, Ulcerogenic medications, Mucus secretion, Bicarbonate secretion
2. What are the goals of treatment? 1-Relieve pain, enhance healing, prevent complications, 2-Neutralize stomach acid, protect mucosa, prevent acid secretion, detect and eradicate H.pylori, 3-Avoid ulcerogenic drugs
3. What are the agents employed against PUD? 1-Antacids, 2-Histamine 2 Receptor Antagonists, 3-Proton Pump Inhibitors, 4-Anticholinergics, 5-Antimicrobials (H.pylori)
4. What is the degree of Acid Inhibition to Heal an Ulcer? It has been observed that a sustained increase in pH (> 4) would be sufficient to heal an ulcer
5. What is one of the risk factors for refractory gastric ulcer? The difficulty of maintaining gastric pH > 4 for a minimum daily period of 16 hr
6. What is the Purpose of Inhibiting Gastric Acid Secretion in cases of Upper GI Bleeding? In upper GI bleeding, the aim is to increase gastric pH in order to prevent acid degradation of the clot & accelerate healing as much as possible.
7. Why is extremely potent inhibition required? To achieve the intended results
8. How should an ideal drug be to achieve a potent acid inhibition? Ideal drug should be able to maintain pH > 4 for ≥ 16 hr/day
9. In what cases is the ideal drug potent inhibition sufficient for? Most refractory cases of peptic acid disease
10. Can potent acid inhibition levels be achieved in all patients? Yes
11. Regardless of what three things in a patient can potent acid inhibition level be achieved? Their basal acid secretion, metabolic capacity, or the presence of absence of H. pylori infection
12. T/F Are Histamine 2 Receptor Antagonists a drug therapy for Treatment of PUD? True
13. What is the mechanism of action of Histamine 2 Receptor Antagonists? It Competitively block the binding of histamine to H2 receptors →reduced intracellular cAMP concentrations →decreased secretion of gastric acid
14. What are the Histamine 2 Receptor Antagonist? (CFNR) 1-Cimetidine, 2-Famotidine, 3-Nizatidine, 4-Ranitidine
15. What is the half-life and dosage of Cimetidine? Cimetidine (Tagamet) half-life=2 hours (800mg QD or 400mg BID)
16. What is the half-life of Famotidine? Famotidine (Pepcid) half-life= 4 hours (40mg QD or 20mg BID)
17. What is the half-life of Nizatidine? Nizatidine (Axid) half-life= 2 hours (300mg QD or 150mg BID)
18. What is the half-life of Ranitidine? Ranitidine (Zantac) half-life= 3 hours (300mg QD or 150mg BID)
19. Does H2-Receptors Antagonists produce 90% reduction in basal & food-stimulated secretion of gastric acid after single dose? Yes
20. Are H2 Receptor Antagonists somewhat less effective in reducing nocturnal secretion? Yes
21. What have studies demonstrated about H2 Receptor Antagonist? Their effectiveness in promoting the healing of DU & GU, & preventing their recurrence
22. Are various H2 receptor blockers equally effective in treating DU and GU? Yes
23. All H2RAs are safe in the treatment of? dyspepsia and PUD.
24. What are the differences between the various H2RAs? Their cost and drug interaction profiles.
25. Which drug out of Ranitidine v. Cimetidine has fewer adverse drug reactions, longer-lasting action, and ten times the activity of cimetidine? Ranitidine
26. Which drug out of Ranitidine v. Cimetidine has 10% the affinity that cimetidine has to P450 so it causes fewer side effects? Ranitidine
27. What H2 blockers have no CYP450 significant interactions? Famotidine and Nizatidine
28. What is the Famotidine activity? 30X Cimetidine
29. What is the equivalent of Nizatidine potency? Ranitidine
30. What is Dyspepsia? chronic or recurrent pain in the upper abdomen or fullness with eating.
31. What can dyspepsia be accompanied by? bloating, belching, nausea or heartburn.
32. What is the cause of dyspepsia? May be due to gastroesophageal reflux disease (GERD) or gastritis > peptic ulcer disease (an ulcer of the stomach or duodenum) > cancer.
33. In H2-Receptors Antagonists, What is the most important determinant of the rate of healing of duodenal ulcers? Suppression of nocturnal acid secretion.
34. What were the previous recommendations for H2RA agents? Administer these agents at least twice a day
35. In H2RA, is a single bedtime dose just as effective & elicit better compliance? Yes
36. When H2RA are administered for 6-8 weeks, what does H2 blockers promote? H2 blockers promote healing of DU in 75% & 90% of cases respectively
37. With appropriate dosages, what is the treatment duration of DU with H2RA in combination with H. pylori eradication therapy? Approximately 4-8 weeks.
38. What heals more slowly, GU or DU? GUs heal more slowly than DUs,
39. Which disease may require an increased duration of treatment of 8-12 weeks? GU
40. What is the pharmacokinetics of H2-Receptors Antagonists? Rapidly absorbed 1-3 hrs to peak
41. What drugs are hepatically metabolized? Ranitidine & Cimetidine
42. What drugs are renally metabolized? Famotidine & Nizatidine
43. Are dose adjustments required in renal & hepatic failure patients? Yes
44. What are the Side Effects of H2-Receptors Antagonists? Usually minor and includes headache, dizziness, diarrhea, & muscular pain
45. Are Hallucinations & confusion in elderly patients some of the side effects of H2RA? Yes
46. What drug is Hepatotoxicity associated with? Ranitidine
47. What drug elevates serum prolactin & alters estrogen metabolism in men? Cimetidine
48. Are Gynecomastia, Galactorrhea and reduced sperm count also some side effects of H2RA? Yes
49. What does the drug Cimetidine inhibit? Inhibits many isozymes of the cytochrome P450 enzyme system
50. What are the isozymes of cytochrome P450 enzyme system that leads to extensive drug interactions? CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4
51. What drugs have no effect on hepatic drug metabolism? Famotidine & Nizatidine
52. What combination with an H2 blocker has questionable rationale? A combination with antacid
53. What is not an appropriate combination with H2-R antagonist? PPIs are not appropriate combination with H2-RA.
54. What drug slows the microsomal metabolism of some drugs in a dose-dependent but in a reversible manner? Cimetidine
55. What does H2RA inhibit the metabolism of? warfarin, diazepam & phenytoin, quinidine, theophylline, carbamazepine, imipramine
56. What drug has less effect on hepatic enzymes? Ranitidine
57. What are the Proton Pump Inhibitors? Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole
58. What is the MOA of PPI? Binds irreversibly to the H+/K+-ATPase enzyme (proton pump) suppressing secretion of hydrogen ions into the gastric lumen
59. Does PPI inhibit both basal and stimulated gastric acid secretion? Yes
60. Are PPIs dose-dependent? Yes
61. What do PPIs inhibit? basal & food acid secretion
62. What is the range in half-life of proton pump inhibitors? 0.5–2 hours
63. Is the effect of a single dose on acid secretion usually persists up to 2–3 days? Yes
64. Do PPIs inhibit the proteolytic activity of pepsin by increasing pH? Yes
65. What are Proton Pump Inhibitors (PPIs) used to treat? Dyspepsia, Peptic ulcer disease (PUD), Gastroesophageal reflux disease (GERD), Laryngopharyngeal Reflux Disease, Barrett's esophagus, prevention of stress gastritis, Gastrinomas and other conditions that cause hypersecretion of acid, Zollinger-Ellison syn
66. T/F Proton Pump Inhibitors (PPIs) are among the most widely-selling drugs in the world as a result of their efficacy and safety? True
67. What are the 1st Generation PPI agents? Omeprazole, Lansoprazole, Pantoprazole
68. What are the 2nd Generation PPI agents? Rabeprazole, Esomeprazole
69. What is Esomeprazoie? Esomeprazole is the S isomer of omeprazole
70. Does Esomeprazoie undergoes less first-pass metabolism in the liver? Yes
71. Does Esomeprazoie have a lower plasma clearance as compared with omeprazole? Yes
72. Do PPIs undergo extensive first-pass metabolism in the liver, resulting in various inactive metabolites that are excreted in the urine or bile? Yes
73. What are PPIs Metabolized by? The cytochrome P450 system (mainly by isoenzymes CYP2C19 & CYP3A4)
74. What are the two generations of PPI? “old” and “new” generations
75. What generation has substantial inter-patient variability in pharmacokinetics? First “old” generation PPIs
76. Does the First “old” generation PPIs have significant interactions with other drugs (CYP 2C19)? Yes
77. What does the time of dosing and ingestion of meals influence? Their pharmacokinetics and their ability to suppress gastric acid secretion.
78. What generation has a relatively slow onset of pharmacological action? First “old” generation PPIs
79. Are first “old” generation PPIs limited in their usefulness in on-demand therapy? Yes
80. Are several doses required to achieve maximum acid suppression in first “old” generation PPIs? Yes
81. Which generation of PPIs fail to provide 24-h suppression of gastric acid? First “old” generation PPIs
82. Does first “old” generation PPIs have nocturnal acid breakthrough even with twice-daily dosing? Yes
83. In “new” generation of PPI, what drugs achieve more rapid and profound inhibition? Rabeprazole and esomeprazole
84. Does “new” generation of PPI, provide acid control and symptom relief over 24 h? Yes
85. In “new” generation of PPI, what is there a balanced metabolism of? Rabeprazole
86. In “new” generation of PPI, what does the metabolism of Rabeprazole involve? Both cytochrome P450 (CYP)-mediated reactions and non enzymatic reactions.
87. In “new” generation of PPI, where does the cytochrome P450 (CYP)-mediated reactions occur? In the liver
88. In “new” generation of PPI, what does a non enzymatic reaction mean? Genetic polymorphisms for CYP 2C19
89. In “new” generation of PPIs, does genetic polymorphisms for CYP 2C19 not significantly influence rabeprazole clearance and clinical efficacy? True
90. What drug is not complicated by clinically significant drug-drug interaction? Rabeprazole
91. What drug is complicated by clinically significant drug-drug interactions? Esomeprazole
92. T/F PPI Inhibition of acid secretion is more pronounced than with H2RAs? True
93. What does the irreversible binding of PPI result in? Prolonged inhibition of gastric acid secretion.
94. T/F PPIs require an acid environment to be effective? True
95. Due to PPIs need of acid environment, should they be used with other antisecretory agents? No
96. When is the dose administered effect of PPIs more effective? Doses administered in the morning result in a higher median 24-hour pH effect than if given at night.
97. In what situations are PPIs more effective? PPIs are effective adjuncts in the eradication of H. pylori (inhibition of the parasites urease activity)
98. What is the treatment duration of PUD with PPIs during appropriate dosages? Approximately 4-8 weeks.
99. Are there any evidence to show that PPIs have direct toxic effects? No
100. What are the most common adverse reactions of PPIs? episodes of diarrhea, nausea, abdominal pain, dizziness, headache, or skin rash
101. How are the manifestations of PPIs? Most often transient & moderate in severity, not requiring reductions in compound dosage
102. In a patient continuously taking PPIs, what deficiency can be apparent? A mild vitamin B12 deficiency has been seen as the result of decreased vitamin absorption
103. What is the reason for the B12 deficiency in patients using B12? This is due to impaired release of the vitamin from food, because this is a process enhanced by the presence of an intragastric acid environment
104. What should be the time of administration of PPIs? Should be administered after fasting (new pumps synthesized overnight) & before a meal so that at the time the peak plasma concentration is reached, there is also a maximum of proton pumps activated (i.e.secreting acid)
105. For treatments of DU & GU, how long should PPIs be used? Should be used for 4-6 weeks
106. How can PPIs have a Short Half-life & a Long-lasting Effect? Despite their short half-life, PPIs exert a persistent pharmacological action b/c they irreversibly binding to the proton pump so they render the necessary synthesis of new enzymes to re-establish gastric acid secretion
107. What is recommended in patients with severe liver failure? A decrease in the usual dose of these drugs is recommended in this group of patients
108. In patients with severe liver failure, what occurs in the area under the plasma curve for PPIs? It increases 7-9 folds
109. In patients with severe liver failure, what happens to the half-life after the PPIs increase 7-9 folds? Their half-life is prolonged to 4-8 hr.
110. Should PPIs influence on phenytoin, carbamazepine, warfarin, & diazepam be monitored? Yes
111. Confirmed by a recent analysis of cases recorded by (FDA), what are the clinical impact of these interactions? It is very low (rates lower than -0.2 per 1,000,000 prescriptions), with no differences between the different PPIs
112. How does the Presence of H. Pylori influence Degree of Acid inhibition? PPIs show a decreased efficacy in patients not infected by H. pylori.
113. What is required for a patient not infected by H. pylori? Due to the decreased efficacy in patients not infected with H. pylori, it requires the use of higher doses of the PPI
114. Do PPIs Have Direct Action on H.Pylori? PPIs inhibit the urease protecting H. pylori from acid
115. How does PPIs work alone? PPIs alone only achieve eradication in 10-15% of cases.
116. Do PPI Promote Actions of Antibiotics in H. Pylori Eradication? PPIs have synergistic effects with several antimicrobial agents
117. What drug increases amoxicillin levels in gastric juices and improve H. pylori cure rate when given with amoxicillin? High dose omeprazole
118. How does clarithromycin activity work against H. pylori? It enhances as gastric pH increases
Created by: sap_213
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