I would like to ask, sometimes the blood vessels on the hands or feet will suddenly become congested and feel very painful. What happened?

This is coagulation dysfunction. Check for low platelet count and insufficient thrombin production.

Vitamin k deficiency (usually lack of thrombin)

Vitamin K is the generic name of 2- methyl-1, 4- naphthoquinone derivatives, which has blood coagulation activity. The natural form is substituted by alkyl side chains in the third position. Vitamin K 1 (chlorophyllin) has a chlorophyllin side chain and is the only homologue of vitamin K found in plants. Vitamin K2 refers to a family of 2- methyl-1 The suffix (-n) indicates the number of isoprene units in the side chain. Menadione is synthesized by bacteria in the intestine, which can supplement some vitamins. Vitamin K is necessary because the core of 1, 4- naphthoquinone cannot be synthesized in vivo.

Vitamin K controls the formation of coagulation factors II (prothrombin), VII (precursor of transformation accelerating factor), VII (coagulation factor, a component of plasma prothrombin kinase) and IX (Stuart factor) in the liver. Other coagulation factors that depend on vitamin K are protein C, protein S and protein Z; Protein C and S are anticoagulants. Protein is two kinds of bone matrix needed for normal bone metabolism, which depends on vitamin K. All these vitamin K-dependent protein contain the amino acid γ-carboxyglutamic acid, and they all participate in the reaction that needs calcium. Vitamin K participates in 10~ 12 glutamic acid residues in prothrombin precursors and is converted into their active forms (prothrombin) by adding carbon dioxide. This addition.

Vitamin K epoxide is the product of vitamin K in glutamyl-carboxylation reaction, which can be recovered as hydroquinone through enzymatic reaction. Coumarin anticoagulants can't block the carboxylation reaction. Instead, they block two reductase enzymes that regenerate from vitamin K epoxide to vitamin K hydroquinone. Because vitamin K hydroquinone is an essential substrate of γ -glutamic acid carboxylase, it cannot be formed, thus inhibiting carboxylation. A large dose of vitamin K( 1~ 10mg) can overcome the blocking of coumarin, and it can regenerate vitamin K hydroquinone by using another reductase in the liver.

The daily requirement of vitamin K is about 65438 0 μ g/kg. Vitamin K deficiency leads to low prothrombinemia, and the concentration of other vitamin K-dependent coagulation factors decreases, showing coagulation defects and bleeding.

Neonatal vitamin K nutrition is dangerous, because: (1) the lipid transported by placenta is relatively insufficient; (2) Immature synthesis of prothrombin in newborn liver; (3) The content of vitamin K in breast milk is low, only 1~3μg/L (5 ~10 μ g/L in milk); (4) It is usually found in postpartum 1~7 days, which can be manifested as bleeding of skin, gastrointestinal tract and intestine. In the worst case, it may be intracranial hemorrhage. The clinical manifestations are the same, which can be seen in postpartum 1~3 months. Usually accompanied by malabsorption and liver disease. If the mother has taken hydantoin anticonvulsants, cephalosporins or coumarin anticoagulants, the risk of these two kinds of hemorrhagic diseases will be high.

Primary vitamin K deficiency in healthy adults is not common. Adults will not lack vitamin K, because vitamin K is widely distributed in animals and plants. Vitamin k circulates and preserves vitamins; Normal intestinal flora synthesizes naphthoquinone. However, vitamin K deficiency can be seen in adults with the lowest dietary intake. If they experience trauma, extensive surgery or long-term parenteral nutrition, whether they receive broad-spectrum antibiotics or not, people with biliary obstruction, malabsorption or substantial liver disease are also at higher risk. People who take certain drugs, including anticonvulsants, anticoagulants, certain antibiotics (especially cephalosporins), salicylates and large doses of vitamin A or E, are very sensitive to vitamin K-related hemorrhagic diseases. People who receive acetyl benzyl hydroxycoumarin should try their best to keep the intake of vitamin K unchanged and avoid the fluctuation of prothrombin level.

Symptoms and signs

Symptoms and signs are caused by low prothrombinemia, which is related to other coagulation factors that depend on vitamin K. Hemorrhage is the main manifestation. No matter due to insufficient dietary intake or the antagonistic effect of drugs on vitamin K, when vitamin K is deficient, it is easy to contusion and mucosal bleeding (especially nosebleed, gastrointestinal bleeding, menorrhagia and hematuria), puncture site or incision bleeding can be seen after trauma, and life-threatening intracranial bleeding can be seen in infants. Obstructive jaundice, if bleeding occurs, usually starts after 4~5 days. The initial bleeding may be from the surgical wound, gums, nose or gastrointestinal tract, or it may be a large amount of gastrointestinal bleeding.

survey fee

The decrease of prothrombin activity and other vitamin K-dependent factors indicates that vitamin K is deficient or antagonistic. Prothrombin time (PT) and partial prothrombin kinase time (PTT) are usually prolonged. Fibrinogen level, thrombin, platelet count and bleeding time were all within the normal range. Normal people who ingest 50~ 150μg of chlorophyllin every day have plasma chlorophyllin levels ranging from 0.2~ 1.0ng/ml. The intake of vitamin K is limited to below 50μ g/d, and the plasma level is generally low. However, only measuring the plasma level without knowing the intake of vitamin K is not helpful for screening deficiency.

The most sensitive indicator of vitamin K deficiency is the appearance of γ-carboxyl prothrombin (DCP) in plasma. DCP, also known as PIVKA (protein induced by vitamin K deficiency or antagonism), can be determined by appropriate antibodies. There is no DCP in plasma of healthy people.

diagnose

According to the symptoms, signs and medical history, the possibility of vitamin K deficiency is suspected. When PT and PTT are prolonged, a diagnosis can be made. Therapeutic trials help to exclude patients with liver disease. If 1mg chlorophyllin dissolved in polyoxyethylene fatty acid IV (also known as vitamin K 1 for injection) is given, the thrombin level can be significantly increased within 2~6 hours. Then it can't be liver disease. [Vitamin K 1 is the generic name of American patent (USP) for chlorophyllin preparation used as medicine, which can be injected or taken orally]. Other diseases, such as scurvy, allergic purpura, leukemia and thrombocytopenia, do not have the characteristics of thrombocytopenia.

prevent

It is suggested that newborns should be given vitamin k 1.5 ~ 1mg+0mg regularly to prevent low prothrombinemia and reduce the incidence of intracranial hemorrhage caused by obstetric trauma. When surgery is considered, it can also be used for prevention. Otherwise, the mother should take a preventive dose (2~5mg/d, oral) of vitamin K 1 before the expected date of delivery. Or give vitamin K 1 solution (2~5mg, intramuscular injection) 6~24 hours before delivery. Pregnant women taking anticonvulsants should take vitamin K 1 20mg every day two weeks before delivery to prevent fetal bleeding. The low chlorophyll content in breast milk is not due to insufficient intake, nor is it stored through fresh leafy vegetables eaten every day.

treat cordially

Chlorophyll quinone is the selected preparation, which is usually called vitamin K 1. Can be used for treating hypoproteinemia, especially hypoproteinemia caused by anticoagulant derivatives of coumarin or indanone. Sodium 2- methylnaphthoquinone disulfide is ineffective against these antagonists because its conversion rate into vitamin K2 is very low (1%). First of all, it is possible that vitamin K 1 should be injected subcutaneously or intramuscularly. The usual dose for adults is 10mg intramuscular injection. In case of emergency, 10~20mg of vitamin K 1 for injection should be dissolved in 5% glucose or 0.9% sodium chloride solution, and injected intravenously at a speed not exceeding 1mg per minute (extremely rare, even if vitamin K 1 is properly diluted and administered slowly, serious allergic reactions can still occur. If the decrease of PT is not satisfactory, the same dose can be used repeatedly within 6-8 hours, generally within 1-2 hours. In most cases, the treatment is effective within 3-6 hours. Patients taking anticoagulants can take vitamin K6550 orally.