mata drugs Flashcards by Elaine Yu

vitamin K1

essential cofactor for g-carboxylation to produce II, VII, IX, X

reverse bleeding episode

SE: dyspnea, chest pain, death

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Tranexamic Acid

fibrinolytic inhibitor

control heavy menses

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Aminocaproic Acid

fibrinolytic inhibitor

reduce bleeding in hemophiliacs

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fibrinolytic inhibitor MOA

competes for Lys binding site on fibrinogen and plasmin to block interaction

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Dipyridamole

phosphodiesterase inhibitor

+warfarin to prevent thrombus on prosthetic heart valves

+aspirin to decrease risk of thrombotic diathesis

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cilostazol

phosphodiesterase inhibitor

treat intermittent claudication

don’t give if CHF

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phosphodiesterase inhibitor MOA

increase intracellular cAMP to decrease platelet aggregation

1) block adenosine uptake
2) inhibit platelet phosphodiesterase

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Ticagelor

ADP inhibitor

equipotent

interacts w/P2Y12 ADP receptor

metabolized by CYP3A4

BBW: bleeding risk

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Prasugrel

ADP inhibitor

greater P2Y ADP antagonism

metabolized by CYP3A4

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Clopidogrel

ADP inhibitor

metabolized vy CYP2C19

poor metabolizers risk CV SE (screen for genotype)

BBW: diminished effectiveness in poor metabolizers

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Ticlopidine

ADP inhibitor

delay in action

1) prescribe w/aspirin
2) give loading dose

BBW: life-threatening bleeding reactions (monitor WBC and platelets)

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ADP Inhibitors MOA

covalently modify/inactivate P2Y ADP receptors

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Tirofiban

platelet GPR blocker

small molecule inhibitor

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Eptifibatide

platelet GPR blocker

small molecule inhibitor

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Abciximab

platelet GPR blocker

monoclonal Ab

irreversibly binds

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platelet GPR blocker MOA + SE

MOA: binds GP IIb/IIIa receptor and prevents interaction w/fibrinogen

SE: bleeding

Aspirin

irreversibly binds COX

efficacy is not dose related

SE: GI bleeding, ulceration

rec: daily baby aspirin

Streptokinase

combines w/plasminogen to create plasmin

SE: Ab production (allergies)

Tenecteplase

tPA

mutated form

longer t1/2

Reteplase

tPA

mutated form

faster onset of action
longer duration of action

Alteplase

tPA

normal human

non-Ag

tPA MOA + SE

MOA: binds fibrin, converts plasminogen to plasmin

SE: bleeding w/cerebral hemorrhage

can have Rx interactions

Warfarin

inhibits epoxide reductase needed to regenerate vitamin K for cofactor synthesis (II, VII, IX, X)

delayed onset (18-24hrs)

CYP2C19 metabolism

narrow therapeutic range (individual dosing)

SE: bleeding, Rx interactions

can be reversed w/vitamin K or transfusion

resistance: VKORC1 gene

Dicumarol

natural anticoagulant in spoiled clover

Dabigatran

direct thrombin inhibitor no monitoring no dose adjustment no Rx interactions greater predictive PK and PD

Argatroban

direct thrombin inhibitor biliary excretion (safe for renal insufficiency)

direct thrombin inhibitor MOA

binds active site of thrombin

Desirudin

hirudin modified form

Bivalirudin

hirudin modified form inhibits platelet activation

Lepirudin

hirudin recombinant form prolonged t1/2 if renal compromise (dose adjustment) SE: bleeding, Ab (anaphylaxis) no reversal agents

hirudin MOA

irreversibly binds thrombin monitor w/PTT

Rivaroxaban

directly inhibits Xa prevents DVT reduces stroke risk premature discontinuation: thrombotic event

low MW heparin MOA + SE

MOA: binds ATIII to inhibit Xa less bleeding longer t1/2 no lab monitoring less risk ITP SE: renal failure

Arixtra (Foundparinux)

binds Xa

unfractionated heparin

MOA: binds ATIII to inhibit Xa and thrombin works on preformed blood components (immediate effect) +thrombolytics for revascularization not IM: risk hematoma not oral: susceptible to acid doesn't cross placental barrier

heparin SE

HAT - heparin associated thrombocytopenia (type 1): direction interaction btwn heparin and platelets causes aggregation HIT - heparin induced thrombocytopenia (type 2): IgG Ab against heparin/platelet complexes cause aggregation SE: bleeding, hemorrhagic stroke