The Detailed Pathology Of Vitamin K Deficiency And Circulating Anticoagulants
Clinical Manifestations Of Vitamin K Deficiency
Vitamin K Deficiency
Vitamin K is essential for the production of functional prothrombin, factor VII, factor IX and X in the liver. In the absence of vitamin K, the blood contains nascent nonfunctional forms of these factors. Nascent nonfunctional forms of protein C also exist in the circulation in vitamin K deficiency. Since the body stores are small, deficiency of vitamin K leads to hypoprothrombinemia within two weeks.
Vitamin K deficiency results from deficient intake, destruction absorption of defective utilization of the liver. Vitamin K deficiency is seen commonly in obstructive jaundice, biliary fistula, malabsorption syndrome, hemorrhagic disease of the newborn, and in overdosage of oral anticoagulants like warfarin or phenindione. Concomitant administration of antibiotics which destroy intestinal flora aggravate the disorder.
Clinically, it manifests as ecchymoses, bleeding from injection sites, bruises, gum bleeding from injection sites, bruises, gum bleeding, hematemesis, melena or hematuria. Both the prothrombin time and activated partial thromboplastin time are prolonged. Administration of vitamin K in a dose of 5-10 mg stops bleeding promptly within 1-2 days. Either the oral water-soluble preparation or parenteral forms may be used. Natural preparations are preferable. If blood loss is severe or response to vitamin K is inadequate, fresh blood transfusion or fresh frozen plasma is also indicated.
Symptomatology Of Circulating Coagulants Deficiency
Sometimes hemorrhagic manifestations develop on account of the presence of anticoagulants in the circulation. Many of these anticoagulants are antibodies to fibrinogen and the other specific clotting substances like factors VIII, IX, V, X, XI and XIII. Antibodies may develop due to repeated transfusions or as part of an immunological disorder like SLE, rheumatoid disease or generalized penicillin allergy.
Clinical features are similar to those of the primary coagulation disorders with the exception that replacement therapy may be ineffective as long as the antibody persists in the circulation. This can be overcome by giving large doses of the missing factor and removal of the circulating antibodies by plasmapheresis or by immunosuppressant therapy.
Heparin is a naturally occurring sulphated negatively charged mucopolysaccharide. It is present in the basophils and mast cells of humans and animals. Heparin binds to antithrombin molecules present in the plasma and on endothelial cell surfaces and accelerates antithrombin inhibition of factors XIIa, Xia, IXa and Xa and thrombin and plasmin. Both PTT and APTT are prolonged. Overdose of heparin causes bleeding which can be reversed by protamine which forms an ionic complex with heparin and prevents its binding to antithrombin. Heparin is used therapeutically to prevent venous and arterial thromboembolism. The ideal is to keep the clotting time 2-2.5 times the normal or APTT to 1.5 to 2 times the normal.
© 2014 Funom Theophilus Makama