Acquired vitamin K-dependent coagulation factor abnormalities

Introduction to acquired vitamin K-dependent clotting factor abnormalities Acquired vitamin K-dependent coagulation factor abnormalities caused by vitamin K deficiency, vitamin K (VK)-dependent coagulation factors and regulatory proteins, including prothrombin, factor VII, factor IX and factor X, protein C (PC) And protein S (PS). The synthesis of these four coagulation factors and regulatory proteins requires vitamin K and may be synthesized in hepatocyte microsomes. basic knowledge Probability ratio: rare, about 0.0014% Susceptible people: no specific population Mode of infection: non-infectious Complications: thrombocytopenic purpura

Abnormal cause of acquired vitamin K-dependent coagulation factor

(1) Causes of the disease

Vitamin K is quite abundant in food, and it has a wide range of sources. The human body needs very little, and it is generally not easy to cause vitamin K deficiency. Vitamin K deficiency can be caused in the following cases:

Malabsorption

Common causes of vitamin K absorption are bile salt deficiency, intestinal absorption function reduction, long-term oral oil lubricants, long-term oral antibiotics to inhibit intestinal bacteria, eating disorders and so on.

2. Oral anticoagulant

Most oral anticoagulants, such as dicoumarin, can accumulate chlorophyllin and cannot be reduced to vitamin K, thus inhibiting the synthesis of vitamin K clotting factors in the body and inhibiting clotting factors by oral anticoagulants. The degree is mainly related to the biological half-life of these clotting factors in vivo. The half-life of factor VII is about 4-6 hours, so it is affected first. The half-life of factor IX is 16-30 h, the factor X is 30-34 h, and prothrombin The half-life is longer, about 36-72 hours, and is usually reduced to the lowest concentration 5 to 10 days after oral administration of the anticoagulant.

(two) pathogenesis

Vitamin K is a coenzyme involved in hepatocyte microsomal carboxylase, which delivers carboxyl groups that rely on vitamin K coagulation factors (prothrombin, factors VII, IX and X) and the amino terminus of protein (protein C and protein S) precursors. The acid residue is carboxylated to form -carboxyglutamic acid.

-carboxyglutamic acid is a molecular structure specific to vitamin K clotting factor, or -carboxyglutamic acid (Gla) structural region. The Gla region is the only amino acid that can bind to calcium ions. The function of clotting factor depends on The binding of these Gla regions to calcium ions; the combined calcium ions bind to the phospholipid surface to activate these coagulation factors, and calcium ions act as a bridge between these glutamic acid residues and phospholipids, but each depends on vitamins. The Gla region of K protein differs depending on the number of glutamic acid residues contained. Factor IX and factor X each contain 12 Gla regions, and prothrombin and factor VII each contain 10 Gla regions, and protein C contains 11 Gla district.

In the absence of vitamin K, the vitamin K-dependent protein synthesized in the liver can become a decarboxylated coagulation factor and protein C and protein S. It is an abnormal protein lacking coagulation biological activity and anticoagulation, but they still have antigen. Sex.

Acquired vitamin K-dependent coagulation factor abnormality prevention

Pay attention to health, do a good job of safety protection, strengthen nutrition, avoid or reduce the use of anticoagulants, reduce and avoid the stimulation and accidental injury of adverse factors, can play a certain preventive role; In addition, early detection, early diagnosis, early treatment is also The key to disease prevention and treatment. In case of onset, active treatment should be actively treated to prevent complications.

Acquired vitamin K-dependent coagulation factor abnormal complications Complications thrombocytopenic purpura

Thrombocytopenic purpura.

Acquired vitamin K-dependent coagulation factor abnormal symptoms Common symptoms Bleeding tendency nosebleed withdrawal reaction gastrointestinal bleeding gum bleeding skin defect skin ecchymosis hematuria

Clinically, there may be bleeding tendency, which is manifested as skin stasis or ecchymosis, nose bleeding, bleeding gums, but the degree of bleeding is generally light, there may be bleeding in the trauma and surgical wounds, in addition, there may be hematuria, menorrhagia , gastrointestinal bleeding, etc., no deep tissue hematoma or joint bleeding.

Examination of acquired vitamin K-dependent clotting factor abnormalities

Prothrombin time and partial thromboplastin time are prolonged, and thrombin clotting time is normal. In severe cases, clotting time and plasma recalcification time may be prolonged.

Diagnosis and differentiation of acquired vitamin K-dependent coagulation factors

According to the medical history, clinical manifestations and laboratory tests are generally not difficult to diagnose.

Attention should be paid to the identification of prothrombin, factor VII, factor IX and factor X deficiency, which can be corrected by prothrombin time correction test and venom time.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.