Pharmacology- clots Flashcards
(45 cards)
what is haemostasis
arrest of blood loss from a damaged vessel
what is exposed when a vascular wall is damaged
collagen and tissue factor (thromboplastin)
what happens in primary haemostasis
platelet adhesion, activation and aggregation (by fibrinogen)
local vasoconstriction
what is the final step of haemostasis
activation of blood clotting and the formation of a stable clot by fibrin enmeshing platelets
what do activated platelets release
thromboxane A2 which causes mediator release (serotonin (5-HT) and adenosine diphosphate (ADP)) and vasoconstriction
what does ADP do
binds to platelet GPCR purine receptors causing;
- further platelet activation
- formation of soft plug
- initiate coagulation of blood and solid clot formation
what converts fibrinogen to fibrin in order to form a solid clot
thrombin
what is thrombosis
a haematological plug in the absence of bleeding
describe aterial thrombus
(white) mainly platelets in fibrin mesh
where do aterial embolis often lodge
in brain
what is the primary treatment of arterial thrombus
antiplatelet drugs (block aggregation and activation of platelets)
describe the components of a venous thrombus
(red) fibrin rich
where do venous embolis often lodge
in lung
what is the primary treatment of venous thrombus
anticoagulants
name six anticoagulants
warfarin, rivaroxiban, heparin, LMWH, dabigatran, fondaparinux
what is the role of vitamin K
mediates enzymes producing clotting factors II, VII, IX and X (precursors of active clotting factors e.g. thrombin= IIa)
what do all anticoagulants carry a risk of
haemorrhage
how does warfarin work
competes with vit k to bind, preventing production of active clotting factors and coagulation
how is warfarin administered
orally
what is the half life of warfarin and why is that important
usually 40 hours (variable)- if patient needs op
how is the overdosage of warfarin treated
with administration of Vit K
why does warfarin have a low therapeutic index
as hard to balance anticoagulant effect and haemorrhage. use complicated by delay to maximal effects and several medical and environmental influences
what can increase risk of haemorrhage with warfarin
liver disease (decreased clotting factors), high metabolic rate (increased clearance of clotting factors), drug interactions
what factors can lessen warfarin action
physiological state (pregnancy, hypothyroidism), vitamin K consumption, drug interactions
