anti-coagulants/anti-platelets Flashcards
indications for anticoagulant drugs
venous thrombosis
atrial fibrillation
which factors does anti-thrombin work against
mostly thrombin and Xa
what is the mechanism of action of heparin
potentiates anti-thrombin
how long does it take for heparin to take effect
immediately
what is the difference between the two forms of heparin
unfractionated
mostly affects thrombin
LMWH
mostly affects Xa
which blood test is used to monitor heparin
APTT
which the of heparin needs monitoring
unfractionated
what are the complications of heparin
bleeding
heparin induced thrombocytopaenia with thrombosis (HITT)
osteoporosis
describe the mechanism of HITT
body recognises heparin as non-self
produces antibodies which create a complex with heparin and platelets
consumptive thrombocytopenia
how does heparin cause osteoporosis
interferes with osteoclasts
how long is the half life of heparin
unfractionated = 30 mins
LMWH = 12-24 hours
which drug can be given to reverse the effects of heparin and how effective is it against the to types of heparin
protamine sulphate
unfractionated = complete reversal
LMWH = partial reversal
what is the mechanism of action of warfarin
vitamin K antagonist
prevents carboxylation of factors II, VII, IX and X making them non-functional
what is needed for the absorption of vitamin K
bile salts
as well as factors II, VII, IX and X, which other substances involved in the clotting system are dependent of vitamin K
protein C and S
why does warfarin have a brief pro-coagulation phase at the start of treatment
it inhibits the action of protein C and S which are naturally occurring anti-coagulants
what is used to monitor warfarin levels
INR
why is INR (modified PT) used to monitor warfarin and not APTT
factor VII has a shorter half life than the other factors affected, so the extrinsic pathway is more acutely changed by changes to warfarin levels
what is the INR
a mathematical correction for differences in the sensitivity of thromboplastin reagent in different centres
what factors influence the risk of haemorrhage in warfarin therapy
intensity of coagulation (increasing INR)
concomitant clinical disorders
drug interactions (including alcohol)
quality of management (reactivity to INR)
examples of mild bleeding on warfarin therapy
skin bruising
epistaxis
haematuria
examples of severe bleeding on warfarin therapy
GI bleeding
intracerebral haemorrhage
significant drop in BP
how long does it take warfarin to leave the system
up to 7 days
how can warfarin therapy be reverse in the event of a bleed
oral vitamin K (6 hours)
IV factor concentrates (immediate effect)
what is the mechanism of action of the NOACs
direct thrombin inhibition (dabigatran)
direct Xa inhibition
(rivaroxaban, apixaban)
what monitoring is required for the NOACs
none
when are NOACs used
post-op thromboprophylaxis
stroke prevention in AF
treatment of DVT/PE
what is the mechanism of action of aspirin
it inhibits cyclo-oxygenase
block production of prostaglandins
prostaglandins needed to produce thromboxane A2 (platelet agonist)
side effects of aspirin
bleeding (nose bleeds, GI bleeding, mucosal membranes)
blocks production of prostaglandins (GI ulceration and bronchospasm)
what is the mechanism of action of clopidogrel/prasugrel
antagonises ADP receptors (prevents platelet aggregation)
which is more potent: aspirin or clopidogrel?
clopidogrel
what is the mechanism of action of dipyramidole
phosphodiesterase inhibitor
reduces production of cAMP which is a secondary messenger in platelet activation
what is the mechanism of action of abciximab
GPIIaIIIb inhibitor
switches off platelet aggregation completely
when is abciximab used
given before heart surgery
how long before an operation should antiplatelet therapy by stopped
7 days
how to reverse anti platelets
platelet transfusion
