1. Pharmacotherapy Preview Program (P3) Antiplatelet Agents Anticoagulants Thrombolytics Lipid Lowering Medications Brandon Dyson, PharmD, BCPS

2. Antiplatelet Agents: What is their purpose and clinical use?

3. Antiplatelet Agents: Mechanism of Action? A B C D

4. Arterial Thromboses: Antiplatelets Matching Aspirin Clopidogrel Ticlopidine Prasugrel Ticagrelor Dipyridamole Abciximab Eptifibatide, Tirofiban A.Binds irreversibly B.Pro-drug, metabolite inhibits P2Y(ADP) C.Metabolized by 2C19 D.Causes thrombocytopenia E.Causes neutropenia F.Very weak platelet inhibitor G.Insufficiently reversed with platelet infusion H.Inhibit the final step in platelet aggregation I.Not a pro-drug, reversible and noncompetitive inhibition of P2Y(ADP)

5. Unfractionated Heparin LMWH – enoxaparin, dalteparin DTI - Argatroban, lepirudin, bivalirudin, dabigatran Fondaparinux, apixaban, rivaroxaban Warfarin Factors A. II B. IIa (Thrombin) C. VII D. IX E. X F. Xa Venous Thromboses Identify the coagulation factors affected by:

6. Venous Thromboses: Warfarin (aka Rat Poison) Explain why warfarin can cause skin necrosis. How do you attempt to prevent this in practice? Why do you have to wait 3-4 days before checking INR for dose adjustments of warfarin? Why does warfarin have so many drug interactions? Discuss the various mechanisms and drug interactions.

7. Henry is an 82 y/o male with a PMH of atrial fibrillation on warfarin. He comes to your office reporting a 3 day history of bright red bleeding from his rectum. Which of the following is the most likely cause of his bleeding episode? A.His wife’s recent trip to the farmer’s market for leafy green kale B.His recent course of antibiotics for URI C.His accidental omission of a dose of warfarin D.His recent cutting back on ETOH use

8. UFHLMWH Monitoring Route of Administration Half-life AE’s and End Organ Damage Clinical Use Monitoring Route of Administration Half-life AE’s and End Organ Damage Clinical Use Compare and Contrast

9. Which of the following regarding the clinical use of unfractionated heparin is FALSE? A.Continuous infusions of heparin require routine aPTT monitoring B.It is the DOC for outpatient DVT prevention post hip and knee replacement surgery C.It is the preferred agent when rapid onset of anticoagulant effects is desired D.It can be chemically antagonized by protamine

10. Which of the following can help break up an existing clot? A.Heparin products B.Fibrinolytics C.Vitamin K antagonists D.Phosphodiesterase inhibitors

11. NOT TESTING MATERIAL. PURPOSE IS TO ENHANCE UNDERSTANDING SO OTHER INFORMATION IS EASIER TO REMEMBER. Cholesterol Synthesis

12. NOT TESTING MATERIAL. PURPOSE IS TO ENHANCE UNDERSTANDING SO OTHER INFORMATION IS EASIER TO REMEMBER.

13. Statins Explain how they work. What time of day should they be taken? Why? How are they metabolized? Which are the two most potent statins? What are the adverse effects? What labs need to be monitored?

14. Bile Acid Sequestrants: Cholestyramine, Colesevelam, Colestipol How do they work? Adverse effects and interactions?

15. Fibrates: Gemfibrozil, Fenofibrate, Clofibrate What is this drug class predominantly used for? What are the side effects? How do they work? What are important DI’s?

17. Niacin Is niacin most effective at improving LDL, HDL and/or triglycerides? What is the most common side effect, and how do you prevent it?

18. Which of the following are correct? A.Bile acid sequestrants often cause flushing B.Ezetimibe reduces cholesterol absorption in the small intestine C.Patients receiving statins should be monitored for changes in serum creatinine due to renal toxicity D.Ezetimibe decreases bile acid reabsorption in the ileum and has GI related adverse effects

19. Which of the following are correct? A.HMG CoA reductase inhibitors are preferred for LDL lowering B.Bile acid sequestrants can greatly reduce TG levels C.Fibrates are more effective at lowering LDL than statins D.Omega-3 fatty acids can greatly reduce TG biosynthesis

20. Patient Case Mr. Pizza is a 55 yo WM with PMH of HTN, diabetes, and 1PPD smoking Meds: Lisinopril, Metformin BP: 135/90 Labs: Total cholesterol 220, LDL 150, HDL 50 (Note: use ASCVD risk calculator for this case) What intensity statin should he receive? What if he was not diabetic and did not smoke?

22. Which of the following are correct? A.Lipid guidelines focus on statin therapy for LDL reduction in high risk groups rather than reaching specific LDL goals B.Patients with clinical ASCVD >75yo should receive high intensity statin therapy C.High intensity statin therapy example is simvastatin 40 mg/day D.Most diabetic patients 40-75yo should receive either moderate or high intensity statin therapy

23. Which of the following patients should receive statin therapy? A.27 year old with primary elevation of LDL = 220 B.35 year old with of LDL = 100 C.History of myocardial infarction D.55 year old with diabetes and LDL = 60 E.45 year old without clinical ASCVD or diabetes with LDL 70-189 and estimated 10-year ASCVD risk of ≥7.5% F.80 year old with diabetes and LDL = 120