Vitamin K Deficiency and Coagulation Factors
Vitamin K deficiency causes deficiencies of functional forms of coagulation factors II, VII, IX, and X (answer B).
Mechanism of Vitamin K in Coagulation
Vitamin K serves as an essential cofactor in the post-translational modification of specific coagulation factors. Its primary role in hemostasis involves:
- Acting as a cofactor for a microsomal enzyme that catalyzes the carboxylation of glutamic acid residues to gamma-carboxyglutamic acid (Gla) in inactive hepatic precursors 1
- This carboxylation is critical for factors II (prothrombin), VII, IX, and X to bind calcium and attach to phospholipid surfaces 2
- Without this carboxylation, these factors cannot participate effectively in the blood coagulation cascade 1
Effects of Vitamin K Deficiency
When vitamin K is deficient, the following occurs:
- Production of non-functional or undercarboxylated forms of factors II, VII, IX, and X 3
- These undercarboxylated factors (also called PIVKA - Proteins Induced by Vitamin K Absence or Antagonism) cannot bind calcium effectively 1
- Without calcium binding, these factors cannot attach to phospholipid surfaces and participate in coagulation 2
- The result is prolongation of prothrombin time and impaired clotting ability 3
Why Other Options Are Incorrect
- Option A (true deficiency of antithrombin): Vitamin K deficiency does not cause antithrombin deficiency. Antithrombin is not a vitamin K-dependent protein.
- Option C (deficiencies of functional forms of fibrinogen and factor VIII): Fibrinogen and factor VIII are not vitamin K-dependent factors, so their function is not directly affected by vitamin K deficiency 4.
- Option D (liver disease): While liver disease can cause coagulopathy and may affect vitamin K metabolism, vitamin K deficiency itself does not cause liver disease 3.
Common Causes of Vitamin K Deficiency
- Fat malabsorption conditions (celiac disease, cystic fibrosis, short bowel syndrome) 3
- Malnutrition 3
- Prolonged antibiotic therapy (disrupts gut flora that produces vitamin K2) 3
- Anticoagulant therapy with vitamin K antagonists (e.g., warfarin) 3
- Neonates (limited hepatic storage) 3
Clinical Manifestations
- Bleeding tendency, which can range from mild to severe 3
- Prolonged prothrombin time (PT) 3
- Normal partial thromboplastin time (unless factors IX and X are severely decreased) 5
- Potentially fatal bleeding, especially in newborns 1
Diagnosis
- Measurement of PIVKA-II (protein induced by vitamin K absence or antagonism-II) - a sensitive biomarker of hepatic subclinical vitamin K deficiency 3
- Prothrombin time and other coagulation tests 3
- Response to vitamin K administration (correction of coagulopathy within 12-24 hours) 2
Treatment
- Vitamin K administration (oral or parenteral) 2
- IV administration has maximum effect in 6-12 hours 3
- Oral supplementation takes about 24 hours for full effect 3
- For severe bleeding, prothrombin complex concentrate may be used alongside vitamin K 3
Prevention
- Adequate dietary intake (leafy greens, cruciferous vegetables, etc.) 3
- Vitamin K prophylaxis in newborns 5
- Monitoring patients on antibiotics or with malabsorption 3
In conclusion, vitamin K deficiency specifically affects the vitamin K-dependent coagulation factors (II, VII, IX, and X), resulting in the production of non-functional forms of these proteins and subsequent coagulopathy.