Gamma-carboxy glutamic acid
Figure 17.4 The carboxylation of the enzyme glutamic acid. This reaction requires vitamin K.
Vitamin K can be depleted through several mechanisms. Because body stores of vitamin K are extremely limited, dietary sources are important. In patients who have prolonged hospitalizations with only parenteral nutrition, dietary deficiency will likely develop and the patient may need to be supplemented. Long-term antibiotic therapy that disrupts normal flora, a source of vitamin K synthesis, may lead to vitamin K deficiency and subsequent bleeding. This is the case only if normal nutrition is also disrupted. Chronic diarrhea, biliary atresia, or other severe liver problems may lead to vitamin K synthesis, because bile salts are needed for proper absorption of vitamin K. Coumadin or warfarin oral anticoagulant therapy reacts because this substance is a vitamin K antagonist and therefore gamma carboxy-lation of factors II, VII, IX, and X is prevented. Patients on oral anticoagulant therapy need to be carefully mon
Drugs That Cause a Deficiency of Vitamin K Clotting Factors itored by anticoagulant clinics and diets need to be modified to compensate for the loss of vitamin K activity. Additionally, there is a long list of drugs that may interfere with vitamin K activity and subsequent hemo-stasis (Table 17.2).
If a patient is vitamin K depleted, the PT and aPTT will most likely be elevated but able to be corrected by normal plasma. Factor assays of the specific vitamin K factors will reveal a depressed activity. Factor VII with the shortest half-life will be depleted first within 2 days; the other factors will take between 3 and 10 days to reach low hemostatic levels. With mild bleeding, oral administration of vitamin K provides hemostatic recovery within a couple of hours. More emergent bleeding situations may result in parenteral administration of vitamin K, blood products, or infusion of prothrombin concentrate complex. An interesting side note is reports of patients who have used coumadin as an agent of suicide.14
Acquired inhibitors of coagulation will be discussed in Chapter 19.
Was this article helpful?