Cardiovascular Drugs (Antithrombotics) Flashcards
Nitrates
nitroglycerine
isosorbide mononitrate
MOA = causes relaxation of smooth muscle in blood vessels resulting in vasodilation
ADP Receptor Inhibitors (irreversible)
clopidogrel (Plavix)
“Pro-drug”
Use = antiplatelet
MOA = active metabolite irreversibly blocks P2Y12 receptor on platelets –> blocks ADP binding –> blocks activation of the GPIIb/IIIa receptor complex –> decreased platelet aggregation.
AE = generally well tolerated; watch out for bleeds, DDI
BOXED Warning = decreased efficacy in some genetic variants –> poor CYP metabolizers
Heparin
Use = anticoagulant
IV, subcut
MOA = Potentiates action of antithrombin which inactivates thrombin and FIXa, FXa, FXIa, FXIIa –> prevents conversion of fibrinogen to fibrin.
AE = monitor for HIT
Reversal agent = protamine sulfate
LMWH
enoxaparin (Lovenox)
IV, subcut
Use = anticoagulant
MOA = potentiates action of antithrombin but has greater effect on inhibiting FXa than thrombin.
Preferred over heparin.
Simple dosing, no monitoring required, decreased risk for HIT
Reversal agent = protamine sulfate and Andexxa
Vitamin K Antagonist
warfarin (Coumadin)
PO
Use = anticoagulant
MOA = binds to VKORC1 –> depletes vitamin K stores –> inhibits synthesis of factors VII, IX, X, II, and protein C and S.
Reversal agent = vitamin K
Risk of intracranial bleed.
Metabolized by CYP2C9.
Does not have immediate effect (3-5 days)
Dosing varies
NTI drug
INR high = thins blood –> bleeding risk
INR low - thickens blood –> clotting risk
Factor Xa Inhibitor
(“-xaban”)
rivaroxaban (Xarelto)
apixaban (Eliquis)
PO
Use = anticoagulant
MOA = selectively and reversibly binds FXa –> stops further coagulation cascade.
AE = less intracranial bleed risk than warfarin, but higher GI bleed risk.
Reversal agent = Andexxa
apixaban has lowest risk of bleed.
Less DDI than warfarin.
rivaroxaban must be taken with high fat meals
HMG-CoA Reductase Inhibitors
(“-statins”)
atrovastatin
pravastatin
rosuvastatin
Use = atherosclerosis
MOA = blocks HMG-CoA reductase = blocks synthesis of cholesterol.
AE = myalgia, dyspepsia, HA, increased liver function enzymes, possible tendinopathy and tendon rupture.
ARNI (Angiotensin Receptor-Neprilysin inhibitor)
sacubitril/valsartan (Entresto)
Use = heart failure
MOA of valsartan = decreased vasoconstriction, aldosterone release, decreased catecholamine release.
MOA of sacubitril = inhibits neprilysin enzyme –> increases natriuretic peptides –> increases vasodilation, diuresis, natriuresis, GFR.
AE = higher risk of angioedema than ARBs; hypotension/dizziness, hyperkalemia
Digoxin
Use = heart failure
MOA = inhibits Na+/K+ ATPase pump in myocardial cells = increased intracellular sodium = increased Ca2+ from Na+/Ca+ exchange pump = increased contractility.
Does not reduce mortality.
Use only if symptoms not controlled with other treatments
Amiodarone
Use = ventricular arrhythmias
MOA = prolong duration of the action potential by blocking K+, Na+, Ca2+ channels; also some beta blocker activity.
AE = liver toxicity, thyroid dysfunction, interstitial pulmonary fibrosis, blueish discoloration on exposed areas of skin.
“LFTs, TFTs, PFTs”
Long half-life (50 days)
