antiplatelets and anticoagulants Flashcards
function of anticoagulants
slow down clotting, by reducing fibrin formation and preventing clots
from forming and growing
examples of anticoagulants
heparin, warfarin
function of antiplatelets
prevent platelets from clumping and also prevent clots from forming
and growing
examples of antiplatelets
aspirin, clopidogrel, ticagrelor, prasugrel
examples of DOACs
apixaban, rivaroxaban, dabigatran
what factors does warfarin act on?
II, VII, IX, X
what factors do DOACs work on
II, X
when should warfarin be given over DOACs
if the patient has mechanical heart valves
how does platelet aggregation occur
inter alia linking of platelets by fibrinogen binding to platelet GPIIb/GPIIIA receptors
what stage do anticoagulants act on
they inhibit the activation of clotting factors and tissue factors
what is the action on fibrinolytic agents (alteplase, reteplase)
they upregulate the activation of plasminogen to plasmin which acts to break down fibrin
how do clots form (pathway)
platelet adhesion activation aggregation -> activation of clotting factors/tissue factors -> fibrin framework arises allowing a thrombus to form
what do antifibrinolytic agents act on and when would they be used?
inhibit plasminogen turning into plasmin - allows clots to form; used to stop excessive bleeding
clotting cascade (draw it out)
https://www.osmosis.org/answers/coagulation-cascade
aspirin mechanism of action
irreversibly inactivates COX-1; alters the balance between thromboxane A2 and PGI2 in the vascular endothelium axis
clinical uses of aspirin
treatment of acute coronary syndrome; stroke (300mg loading dose); secondary prevention of arterial thrombosis (long term) after CV events; analgesia (much higher dose)
adverse effects of aspirin
GI bleed (due to PGs action in mucous barrier building); bronchospasm
MOA of clopidogrel
irreversibly inhibit the binding of ADP to the receptor on platetlets, inhibiting ADP-mediated platelet activation and GP IIb/IIIa mediated platelet aggregation
MOA of prasugrel
irreversibly inhibit the binding of ADP to the receptor on platetlets, inhibiting ADP-mediated platelet activation and GP IIb/IIIa mediated platelet aggregation
MOA of ticagrelor
reversible, non-competitive, P2Y12 inhibitor
clinical use of antiplatelets (clopidogrel, ticagrelor etc. - 3)
prophylaxis and treatment of MI, stroke and other vascular disorders
adverse effects of antiplatelets (5)
bleeding; GI discomfort; rashes; neutropoenia; dyspnoea (rare)
MOA of alteplase, duteplase, reteplase & streptokinase
activate plasminogen (acting as an enzyme) to form plasmin which digests fibrin and fibrinogen which dissolves the clot
what must be checked before thrombolysis
the stroke is not haemorrhagic
use of thrombolytic agents (alteplase etc. - 4)
MI; ischaemic stroke; arterial thrombosis; occaionally in DVT/PE
why should thrombolytic agents not be used after the initial dose
antibodies appear after the initial dose (around 4 days after) which can block the action of the drugs
adverse effects of thrombolytic agents
bleeding; reperfusion dysrhythmias; nausea/ vomiting; hypersensitivity reactions
MOA of tranexamic acid
inhibits plasminogen activation, preventing fibrinolysis (opposite to alteplase)
use of tranexamic acid
reduction of haemorrhage
why might heparin have to be distributed multiple times?
it has a short half life
MOA of heparin
accelerates action of antithrombin III - results in downregulating clotting factors IIa and Xa (also affects IXa, XIa & XIIa)
clinical uses of heparin (3)
treatment of vein thrombosis/PE; unstable angina; PAD
adverse effects of heparin (4)
bleeding; thrombocytopaenia; hypersensitivity reactions; osteoporosis
MOA of LMWH - enoxaparin, dalteparin, bemiparin
accelerate action of antithrombin III (inactivates factor Xa)
clinical uses of LMWH (4)
prophylaxis of VTE; treatment of DVT/PE; treatment of MI; treatment of angina
why use LMWH rather than heparin (3)
better bioavailability; longer half life; less likely to cause thrombocytopaenia, hypersensitivity and osteoporosis
how to treat LMWH overdose
protamine sulphate
what drug class if warfarin
anticoagulant
MOA of warfarin
Vit K antagonist - inhibits the reduction of vit K (thus preventing the carboxylation of glutamate residues in factors II/VII/IX/X)
clinical use of warfarin (2)
treat VT/PE; prophylaxis of embolism in AF & valvular heart disease
when should warfarin be given over DOACs
if mechanical heart valves are present
adverse effects of warfarin
bleeding - treat by giving vit K or prothrombin complex concentrates
what must be monitored for warfarin
INR (prothrombin time)
rivaroxiban; apixaban; dabigtran drug class
factor Xa inhibitors; DOACs
dabigatran MOA
direct inhibitor of clot-bound and free thrombin (factor IIa)
rivaroxiban, apixaban MOA
direct factor a inhibitors
cons of dabigatran
low bioavailaibility - 80% excreted renally
rivaroxiban; apixaban; dabigtran clinical use
prophylaxis of DVT/PE in ortho surgery; treatment of VTE; prophylaxis of stroke in AF
what should be given for a haemorrhagic stroke
anti hypertensives e.g. labetolol
what should be done if AF + acute coronary syndrome is present
triple therapy (e.g. fondaparinux, aspirin/clopidogrel, ticagrelor)
