anticoagulation Flashcards
what is the role of prostacyclin?
released by endothelial layer of blood vessels, to stop the sticking of platelets to the blood vessel wall
what is the role of nitric oxide gas in blood vessels?
it is released by endothelial layer of blood vessels to prevent sticking of platelets to the blood vessel wall and helps blood pressure regulation.
what is the action of warfarin?
it is a vitamin K antagonist
inhibits vitamin K reductase which is needed by vitamin K to turn inactive prothrombin into thrombin.
what is a DOAC?
an oral thrombin inhibitor (thrombin is the enzyme that converts fibrinogen into fibrin)
why is the disadvantage of DOACs compared to warfarin?
DOACs cannot be reversed, warfarin can be reversed by taking vitamin K
what is the role of heparins?
as warfarin takes a few days to take effect, , enoxaparin (a heparin) Is taken until it takes effect.
why are heparins like enoxaparin not taken in long term?
they are uncomfortable to inject and taking enoxaparin every day would lead to platelet depletion
where is arachidonic acid found?
in all cell membranes, it is chopped out of the cell membrane when cell is excited.
what is the role of arachidonic acid?
it is converted by the COX enzyme into prostaglandins.
what does prostaglandins do?
cause constriction of the airways
what does prostacyclins do?
in blood vessel endothelial cells, they are antiplatlets and vasodilators 3
what does thromboxane do?
in platelets, it increases aggregation
what does nitric oxide do?
it is a gas that is released by the endothelial cells of the blood vessels and they help with blood pressure regulation and prevent platelets sticking to the blood vessel wall by increasing platelet cGMP
what are the steps in the arachidonic acid pathway?
arachidonic acid in all cell membranes > free arachidonic acid > endoperoxides > prostaglandins > prostacyclins / thromboxane
what is the action of low dose aspirin?
it is a COX inhibitor.
it prevents the reaction of free arachidonic acid to endoperoxides.
so stops prostacyclin formation and thromboxane formation.
this is bad as you want a low level of thromboxane but you don’t want prostacyclin levels to deplete.