Vitamin K
last authored: June 2010, Krista McLellan
last reviewed:
Introduction
Vitamin K, or phytonadione, is an important cofactor in the clotting cascade.
Daily Requirements
Vitamin K is effectively recycled in the liver, and the daily dietary requirement is low. Endogenous bacterial flora also readily synthesize the vitamin.
Sources
There is still a small but definite need for dietary vitamin K, which is widely available in our food:
- green leafy vegetables
- liver
- vegetable oils
Biological Roles
Vitamin K's principle role is in the post-translational modification of of clotting factors. It acts as a cofactor for a liver enzyme (microsomal carboxylase) which adds a carboxyl group to clotting factors II, VII, IX, and X (mnemonic: 1972).
Carboxylation adds calcium binding sites and allows the calcium-dependent interaction of these factors with phospholipid surfaces on platelets and endothelial cells.
Activation of protein C and protein S, protein Z also require vitamin K.
In recent years, a wide variety of non-coagulation involved proteins have also been shown to depend on vitamin K. These proteins are found in kidney, bone, placenta, and lung. One protein, osteocalcin in bone, may suggest vitamin K has a role in promoting bone calcification.
Deficiency
Deficiency can occur:
- in neonates, whiose liver reserves are small
- in fat malabsorption syndromes
- after destruction of vitamin K-synthesizing flora
- in diffuse liver disease
Bleeding disorders can result, characterized by hematomas, hematuria, melena, ecchymoses, and bleeding from the gums. Not petechiae.
An estimated 3% of neonates experience vitamin K deficiency and subsequent bleeding, warranting prophylactic vitamin K therapy. Within a week, endogenous flora produce sufficient amounts.
Overdose
In patients with thromboembolic disease, vitamin K levels are decreased using warfarin, which blocks the activity of liver enzyme epoxide reductase and prevents vitamin K regeneration.
Vitamin K toxicity can result in jaundice.
Resources and References
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