1 / 59

Comprehensive Review of Prostaglandins, Thromboxanes, and COX Inhibitors

This review covers crucial topics related to prostaglandins (PGs) and thromboxanes (TXs), including their structures, functions, signaling pathways, and clinical implications. Key physiological roles such as blood pressure regulation, wound healing, and reproductive processes like ovulation and labor are discussed. The review also explores COX enzymes (COX-1, COX-2) in drug interactions, the mechanisms of NSAIDs, and the effects of enhanced lipophilicity on drug metabolism. A detailed analysis of 57 questions aids in mastering these complex biochemical topics.

adara
Télécharger la présentation

Comprehensive Review of Prostaglandins, Thromboxanes, and COX Inhibitors

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Review for the Test

  2. The Test • 57 Questions/Need to Answer 55 • 27 My Section • 9.30-11.30p? • 1-2 minutes/question

  3. COX-2 Physiological Role • Renin-angiotensin system • blood pressure and fluid balance • Ovulation and labor • Wound healing • Vascular endothelium • Vascular remodeling

  4. Modified PGs (mostly) • Block w-oxidation • Methyls at 15 and/or 16 • Phenyl in 17-20 range • Increase Lipophilicity • Add methyls, phenyls and esters

  5. ADME: Metabolism E b E b 15 14 15 E Prevents Beta-oxidaton R 13 b O D w G 14 E R 13 O b R 14 13 Talfuprost E=Esterase, O=Oxidation, R=Reduction, b=b-Oxidation, w=w-Oxidation, D=dealkylation, G=glucuronidation

  6. Overview • Prostaglandins (PGs) and Thromboxanes (TXs) • NSAIDs • Gout

  7. PGs and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  8. What Prostaglandin is this? • PGE1 • PGE2 • PGF2alpha • PGG2 • PGH2 • PGI2 • TXA2 :10

  9. What Prostaglandin is this? • PGE1 • PGE2 • PGF2alpha • PGG2 • PGH2 • PGI2 • TXA2 :10

  10. What Prostaglandin is this? • PGE1 • PGE2 • PGF2alpha • PGG2 • PGH2 • PGI2 • TXA2 :10

  11. PG and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  12. Select the one that is not true • PGE2 relaxes vascular smooth muscle • TXA2 increases renal blood flow • PGI2 protects the gastric mucosa • PGF2alpha contracts uterine smooth muscles • PGF2alpha causes bronchoconstriction :10

  13. PG and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  14. Prostaglandin signaling within the cell is? • Endocrine • Autocrine • Paracrine • Intracrine :10

  15. What are not involved in Prostaglandin and Thromboxane signaling • Plasma membrane bound GPCRs • Nuclear membrane bound GPCRs • Nuclear Receptors • OATP transporter :10

  16. Prostaglandin E2 (PGE2) binds to what type of receptor • DP1 • EP1 • FP • IP • TP :10

  17. PG and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  18. What ways are PG and TX transported • Active Efflux • Active Influx • Passive Diffusion • All the above :10

  19. PG and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  20. The substrate of COX 2 is? • Arachidonic Acid • PGE1 • PGE2 • PGF2alpha • PGG2 • PGH2 • PGI2 • TXA2 :10

  21. The product of COX 2 is? • Arachidonic Acid • PGE1 • PGE2 • PGF2alpha • PGG2 • PGH2 • PGI2 • TXA2 :10

  22. What is not a mechanism of metabolism for PG? • alpha-oxidation • beta-oxidation • omega-oxidation • reduction • alcohol dehydrogenation :10

  23. How is TXB2 produced • reduction • oxidation • hydrolysis • conjugation :10

  24. Which Cytochrome P450 (CYP) is involved in w-oxidation? • CYP1A1 • CYP2C9 • CYP3A4 • CYP4A :10

  25. PG and TXs • Structures • Functions • Signaling • Transport • Synthesis and Degradation • PG as drugs

  26. NSAIDs will interfere with PG drugs because they can • Inhibit PG synthetases • Induce COX 2 expression • Reduce COX 2 expression • Inhibit COX 1 • Inhibit COX 2 • D and E :10 diclofenac

  27. What prostaglandin is Aprostadil? • PGE1 • PGE2 • TXA2 • Prostacyclin only • PGI2 only • Prostacyclin and PGI2 :10 Aprostadil

  28. What is not a use of Aprostadil • Erectile dysfunction • Congenital hear defect • Hypertension • Induce labor • A and B • C and D :10

  29. Aprostadilbinding to a GPCR causes all but the following • Increase intracellular Ca2+ • Decrease intracellular Ca2+ • Activate adenylatecyclase • Increase cAMP :10

  30. What are not formulations of Alprostadil? • IV injection • Penile injection • Oral • Urethral Suppository :10

  31. What are ADR of Alprostadil? • Pain/Rash • Light Headed • Bleeding and Bruising • Flu Symptoms • All the above :10

  32. Talfluprost

  33. The compounds on the previous pagearemodified versions of what prostaglandin? • PGE1 • PGE2 • TXA2 • PGF2a • PGI2 • 15-methyl PGF2a :10

  34. Overview • Prostaglandins (PGs) and Thromboxanes (TXs) • NSAIDs • Gout

  35. NSAIDs • COX 1, COX 2 and COX3 • COX 1/COX 2 IC50 ratios • COX 1 and COX 2 inhibitor side effects • Cancer • Structural Classes of NSAIDs

  36. NSAIDs will inhibit [blank] in a patient • COX 1 • COX 2 • COX 3 • COX 1 and COX 2 • COX 1, COX 2 and COX 3 :10

  37. COX 3 should be considered with NSAID therapeutic regiments. • True • False :10

  38. COX 1 has a larger active site than COX 2. • True • False :10

  39. NSAIDs • COX 1, COX 2 and COX3 • COX 1/COX 2 IC50 ratios • COX 1 and COX 2 inhibitor side effects • Cancer • Structural Classes of NSAIDs

  40. A new COX inhibitor has a COX-1/COX-2 IC50 ratio of 0.1. What COX enzyme is it selective for? • COX-1 • COX-2 • Non-specific • COX-3 :10

  41. NSAIDs • COX 1, COX 2 and COX3 • COX 1/COX 2 IC50 ratios • COX 1 and COX 2 inhibitor side effects • Cancer • Structural Classes of NSAIDs

  42. Inhibition of PG leads to all but the following in the GI tract • Increase HCO3 • Increase in H+ • Increase in mucus • Decrease in mucus • A and B • B and C • A and C :10

  43. What are not COX 1 side effects • GI bleeding • Hypotension • Clotting disorders • Bronchodilation • A and B • B and C • B and D :10

  44. PG inhibition leads to bronchoconstriction through • PGE2 • PGE1 • PGG2 • Leukotrienes (LT) • TXA2 :10

  45. What type of adverse side effects do you anticipate by interfering with renin-angiotensin system through COX-2 inhibition? • Hypertension • Hypertension and Renal Failure • Renal Failure • Brain Damage • None of the above :10

  46. NSAIDs • COX 1, COX 2 and COX3 • COX 1/COX 2 IC50 ratios • COX 1 and COX 2 inhibitor side effects • Cancer • Structural Classes of NSAIDs

  47. What are non COX 2 functions for NSAIDs in Cancer cells? • Block NF-kappaB signaling • Activate Peroxisome proliferator receptor • Increase Apoptosis • Activate NF-kappaB signaling • A, B and C • All the above :10

  48. Which drug is non-selective for COX 1 and COX 2 • Low dose Aspirin • High dose Aspirin • Ibuprofen • Celecoxib • All the above • B and C :10

  49. What is not a structural class of NSAIDs? • Salicylates • Profens • Fenacs • Oxicams • Statins :10

  50. Salicylates inhibit by the following mechanisms • Competitive • Irreversible • Non-competitive • Uncompetitive • A and B • B and C • All the above :10

More Related