Download NURO 544 Module 8 Cardiology II

Pharmacotherapy Preview
Program (P3)
Antiplatelet Agents
Anticoagulants
Thrombolytics
Lipid Lowering Medications
Brandon Dyson, PharmD, BCPS
Antiplatelet Agents:
What is their purpose and clinical use?
Antiplatelet
Agents:
Mechanism
of Action?
A
B
C
D
Arterial Thromboses:
Antiplatelets Matching
•
•
•
•
•
•
•
•
Aspirin
Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor
Dipyridamole
Abciximab
Eptifibatide,
Tirofiban
A.
B.
C.
D.
E.
F.
G.
Binds irreversibly
Pro-drug, metabolite inhibits P2Y(ADP)
Metabolized by 2C19
Causes thrombocytopenia
Causes neutropenia
Very weak platelet inhibitor
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)
Venous Thromboses
Identify the coagulation factors affected by:
• 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:
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.
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
Compare and Contrast
UFH
LMWH
• Monitoring
• Monitoring
• Route of Administration
• Route of Administration
• Half-life
• Half-life
• AE’s and End Organ Damage
• AE’s and End Organ Damage
• Clinical Use
• Clinical Use
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
Which of the following can help break
up an existing clot?
A.
B.
C.
D.
Heparin products
Fibrinolytics
Vitamin K antagonists
Phosphodiesterase inhibitors
Cholesterol Synthesis
NOT TESTING MATERIAL. PURPOSE IS TO ENHANCE UNDERSTANDING SO OTHER INFORMATION IS EASIER TO REMEMBER.
NOT TESTING MATERIAL. PURPOSE IS TO ENHANCE UNDERSTANDING SO OTHER INFORMATION IS EASIER TO REMEMBER.
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?
Bile Acid Sequestrants:
Cholestyramine, Colesevelam,
Colestipol
How do they
work?
Adverse effects
and interactions?
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?
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?
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
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
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?
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
Which of the following patients should
receive statin therapy?
A.
B.
C.
D.
E.
27 year old with primary elevation of LDL = 220
35 year old with of LDL = 100
History of myocardial infarction
55 year old with diabetes and LDL = 60
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