Acquired coagulation factor disorders
- Mechanism
Most clotting factor problems are acquired: too little vitamin K, a failing liver, antibodies against a factor, or venom that eats fibrinogen.
What it is
Acquired coagulation defects usually affect several factors at once. Vitamin K is needed to γ-carboxylate factors II, VII, IX and X and proteins C and S; deficiency follows poor intake, fat malabsorption, antibiotics that kill gut flora, newborn status or vitamin K antagonist drugs and rodenticides. The liver makes most clotting factors, so severe liver disease causes complex bleeding. Autoantibodies against a single factor (acquired haemophilia, usually against factor VIII) are rare but dangerous. Venom of Bothrops snakes, the commonest venomous bites in Colombia, activates and consumes fibrinogen and other factors.
Step by step
- Vitamin K is absent or blocked (warfarin, superwarfarin rodenticides) or the liver cannot synthesize factors.
- Factors are made but not γ-carboxylated, so they cannot bind calcium and phospholipid surfaces.
- PT prolongs first (factor VII), then PTT as other factors fall.
- Alternatively, venoms or DIC consume fibrinogen and factors faster than the liver replaces them.
- Bleeding appears from mucosae, wounds, gut and brain.
Acquired coagulation defects
| Cause | Mechanism | Typical tests | Context |
|---|---|---|---|
| Vitamin K deficiency or antagonists | No γ-carboxylation of II, VII, IX, X | Long PT, then long PTT; corrects with vitamin K | Newborns, malabsorption, antibiotics, warfarin, rodenticides |
| Liver disease | Reduced synthesis of most factors | Long PT and PTT, low fibrinogen, low platelets | Cirrhosis, acute liver failure |
| DIC | Consumption of factors and platelets | Long PT and PTT, low fibrinogen, high D-dimer | Sepsis, obstetric emergencies, cancer |
| Acquired factor inhibitor | Autoantibody, usually against factor VIII | Long PTT not corrected by mixing | Older adults, postpartum, autoimmune disease |
| Bothrops snakebite | Venom enzymes consume fibrinogen | Incoagulable blood, very low fibrinogen | Rural Colombia and Latin America |
Clinical notes
- Vitamin K deficiency bleeding of the newborn can be early, classic or late (intracranial); prophylaxis at birth prevents it.
- Antivenom, not plasma alone, reverses Bothrops coagulopathy.
Test yourself
Think of the answer, then tap the question to see it.
Which factors depend on vitamin K?
Factors II, VII, IX and X, and the anticoagulant proteins C and S.
Why is the PT the first test to prolong in vitamin K deficiency?
Factor VII has the shortest half-life, and the PT is most sensitive to it.
How does Bothrops venom cause bleeding?
Its enzymes activate and consume fibrinogen and other factors, leaving the blood unable to clot.
Elsewhere in DurgiPedia
- Vitamin K (phylloquinone)
- Vitamin K epoxide reductase (VKORC1)
- The coagulation cascade
- Coagulation tests: PT/INR, aPTT and platelets
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Vitamin K deficiency bleeding of the newborn: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Vitamin K: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.