11.2 Anticoagulants Flashcards
how is antithrombin 3 linked to clotting factors?
endogenous inactivator of CFs
how are coagulation factors in the blood? benefit?
zymogens
activated locally for fine control
function of purple blood tube
EDTA chelates calcium, prevents sample clotting
function of blue blood tube
can add calcium back in to get a clotted sample if needed
pharmacodynamics of UFH
fast onset,
half life 30mins-2 hours
unpredictable elimination
how is UFH able to catalyse inhibition of 2a?
binds simultaneously to 10a and 2a
example of LMWH, and a synthetic version
dalteparin
fodaparinux
half life of LMWH
over 2 hours, more predictable
why could heparins cause hyperkalameia
inhibit aldosterone secretion
contraindications of heparins
clotting disorders
renal impairment
DDIs for heparins
other antithrombotics
ACEi/ARB or K+ sparing, due to hyperkjalameia
how is UFH titrated?
activated partial thromboplastin time
vit K antagonist mechanism of action
competitive inhibition of VKOR
vit k dependent clotting factors
which is most sensitive? usefulness?
2.7.9.10
7, used in prothrombin time
why might there be a delayed onset of action for vit K antagonists?
circulating active clotting factors are present for several days, need to be cleared and replaced with inactive forms
link warfarin and NSAIDs
NSAIDs decrease GI absorption of vit K, increase INR so more anticoagluated so high bleed risk
INR target for DVT, PE, AF
2.5
INR target is recurrent DVT or PE and on anticoagulants
3-3.5
how do the 2 classes of DOACs work? give example drugs
direct Xa inhibition, inhibit both free Xa and that bound with antithrombin 3, not directly affecting 2a
e.g. apixaban, rivaroxaban
direct competitive 2a inhibitor, circulating and thrombus bound
e.g. dibigatran
benefits of DOACs
oral, little direct monitoring, take at home
DOAC ADRs
bleeding
skin reactions
AF score for DOAC
ORBIT/HASBLED
contraindications of DOAC
low creatinine clearance for dibigatran
pregancy
DDIs for DOAC
CYP inhibitors/inducers
