Blood Clotting Affected by Warfarin: Concept Map and Summary

Running head: CONCEPT MAP 1
Blood clotting affected by warfarin
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CONCEPT MAP 2
Introduction
The clotting system involves a process where blood forms clots following a tissue injury
to prevent further blood loss(Gee, 2018). The process follows a coagulation cascade where
various clotting factors are involved(Gee, 2018). There are two major pathways of the
coagulation which include the intrinsic and extrinsic pathways. There are several coagulation
factors that are involved in both pathways which include the tissue factor, factors XIII, XII, XI,
X, IX, VIII, VII, V, IV, III, II and I(Tshikudi, Tripathi, Hajjarian, Van Cott & Nadkarni, 2017).
Other important factors include calcium ions and vitamin K(Gee, 2018). Vitamin K is involved
in activation of various coagulation factors. Warfarin work against as vitamin K hence it can
inhibit the whole process resulting in homeostasis imbalance(Tshikudi, Tripathi, Hajjarian, Van
Cott & Nadkarni, 2017).
Blood clotting affected by warfarin
The blood clotting cascade is influenced by various clotting factors and cofactors. The
cofactors are usually the inactive form of certain factors that activates various clotting factors
into active forms(Palta, Saroa & Palta, 2014). Failure of this activation, no blood clotting can
occur(Gee, 2018). Vitamin K is one of the cofactors used to activate the clotting factors X, IX,
VII and II. An increased activation of vitamin K will lead to increase in clotting process and vise
vasa(Gee, 2018).
Therefore, VItamin K acts as an important contributing factor of the clotting process due
to its effects on its dependent factors of the coagulation cascade(Goodman, Brunton, Chabner &
Knollmann, 2012). This is due to the fact that, Vitamin K form one of the major factor that is
required by the liver microsomal enzyme known as vitamin K epoxide reductase (VKOR) that
catalyzes the conversion of the specific glutamyl precursors of the vitamin K clotting factors to

CONCEPT MAP 3
gamma-carboxyl glutamyl residues in a plasma form of these proteins(Goodman, Brunton,
Chabner & Knollmann, 2012). The product that comes from this carboxylation reaction is the 2,
3 eporoxide of Vitamin K quinone. Warfarin, which acts as the Vitamin K inhibitor is made up
of the mixture of S- and R- enantiomers(Palta, Saroa & Palta, 2014).
The S- warfarin is usually the most active type of enantiomer than the R-warfarin. Both
warfarin enantiomers inhibit the process of coagulation by blocking the enzymes encoded as
VKORC1(Malátková, Sokolová, Chocholoušová Havlíková & Wsól, 2016). This, in turn, read to
the reduction of peroxides of the vitamin K or oxidized vitamin K into an active coenzyme of the
vitamin known as hydroquinone(Goodman, Brunton, Chabner & Knollmann, 2012). Since
vitamin K serves a major cofactor of glutamyl carboxylase that serves as the catalyst in the
carboxylation process of factors X, IX, VII and II, this characteristic of Warfarin decreases the
activity of all carboxylated clotting factors that are dependent on vitamin K(Harter, Levine &
Henderson, 2015).
Calcium ions that usually activate prothrombin to thrombin normally function well in the
presence of gamma carboxyl glutamyl in order to form des-gamma-carboxyl forms of
prothrombin. Thereby, only the activated vitamin K can act as a cofactor in the conversion of
prozymogens into zymogens capable of binding with calcium ions and smoothly interacting with
phospholipids surfaces(Goodman, Brunton, Chabner & Knollmann, 2012). Therefore, the
introduction of warfarin normally reduces the blood thrombotic potential as the needed factors
are inactivated. The reduced vitamin K can be held back into normal through the intake of more
vitamins K in the body and reduced dose of warfarin(Malátková, Sokolová, Chocholoušová
Havlíková & Wsól, 2016). Below is the concept map that summarises the above whole process.