Vitamin K contributes to the synthesis of several proteins used in coagulation, including factors II, VII, IX, and X. It works as a cofactor in the carboxylation of glutamic acid residues on prothrombin complex proteins. The deficiency of this vitamin will manifest with mucocutaneous bruising or bleeding.
Neonates are at risk of developing vitamin K deficiency because they lack the gut bacteria that produce vitamin K. It is also not present in breast milk. It is diagnosed via the presence of neonatal hemorrhage and/or increased PT and aPTT. Neonatal hemorrhage can manifest on days 2-7 of life, resulting in mucocutaneous bleeding (e.g., epistaxis), easy bruising, gastrointestinal bleeding, and/or intracranial hemorrhage.
Severe liver disease is associated with fat malabsorption, which reduces the absorption of vitamin K. Deficiency can occur in 7-10 days in acutely ill patients with liver disease.
Chronic use of broad-spectrum antibiotics, especially cephalosporins, will reduce vitamin K's absorption in the body. This occurs due to the antibiotics killing bacteria that contribute to vitamin K production in the gastrointestinal tract. In addition, N-methylthiotetrazole side chains on cephalosporins are hepatic vitamin K epoxide reductase inhibitors, resulting in a deficiency of vitamin K.
Patients taking vitamin K antagonists such as warfarin may be at risk of developing vitamin K deficiency. Severe deficiency can occur if the patient experiences rat poison intoxication, as this acts similarly to warfarin.
Vitamin K is fat-soluble. Disorders leading to impaired fat absorption will reduce the absorption of vitamin K. Those disorders include cystic fibrosis, biliary disease, pancreatic disease, celiac disease, and Crohn's disease.
The primary sources of vitamin K for the body come from the diet and from intestinal bacterial production. Dietary deficiency of vitamin K is rare in healthy individuals and takes several weeks or months to occur. However, severely malnourished patients and heavy drinkers are at risk of developing this condition.
Bleeding Time (BT) is a marker of platelet function. Because vitamin K deficiency doesn't affect platelets, patients can have a normal bleeding time.
Vitamin K deficiency will reduce the synthesis of coagulation factors II, VII, IX, X, protein C, and protein S. This will result in an increased prothrombin time (PT), which is a marker of the extrinsic pathway of coagulation, and increased partial thromboplastin time (PTT), which is a marker for the intrinsic pathway of coagulation.
Due to the lack of production of vitamin K in neonates, a vitamin K injection is given at birth to prevent hemorrhage.
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