Peptic Ulcers, Headache, Antiemetic drugs

1.     Explain why persons with hereditary angioedema experience attacks of angioedema. Refer to kallikrein, bradykinin and complement C1 inhibitor.

2.     Explain why the use of an ACE inhibitor in a person with hereditary angioedema may be dangerous.

3.     Explain why diphenhydramine or scopolamine are useful in the nausea and vomiting of pregnancy motion sickness.

4.     Describe the different mechanisms by which haloperidol and ondansetron diminish the nausea and vomiting of cancer chemotherapy.

5.     Explain why cisplatin is more emetogenic than other cancer chemotherapy drugs and why ondansetron or granisetron are particularily effective at decreasing cisplatin induced nausea and vomiting.

6.     Use the diagram on the Key for the Applied Learning to illustrate your responses to items 3-5.

7.     Describe the effects of stimulating H1 and H2 histamine receptors on the body.

8.     List the important cells in the stomach that are involved in the production of stomach acid and mucus.

9.     Describe the normal physiological factors, in particular the ligands and receptors, that affect the secretion of stomach acid and mucus.

10. Explain how he following drugs might be useful in peptic ulcer disease because of their effects on parietal cells or stomach acidity:  histamine H2 blocking drugs, protein pump inhibitors, antimuscarinic drugs, sulcralfate, misoprostol, antacids.

11. Note which of the drug categories in the preceding item have documented efficacy in promoting the healing of peptic ulcers.

12. Give two examples each of histamine H2 blocking agents and protein pump inhibitors.

13. State the role of Helicobacter pylori in peptic ulcer disease and explain why antibacterial such as Pepto Bismol, metronidazole and tetracyclines might be used in peptic ulcer disease.

14. Describe a significant problem with the continuous use of proton pump inhibitors when they are not really needed.

15. Summarize the serotonin-platelet hypothesis of migraine and the neuroinflammatory hypothesis of migraine.

16. In light of those hypotheses explain the antimigraine action of the tryptans and ergotamine.

17.  Compare the adverse effects of ergotamine and tryptans to illustrate why the tryptans have replaced ergotamine as the treatment of choice for acute migraine headache.

18. State the physiologic effects of stimulating and blocking the following serotonin receptors:   5HT1D/1B,  5HT3,  5HT2B