Fibrinogen deficiency

The fibrinogen molecule is 30 times as long as it is broad. This asymmetry is responsible for the increased viscosity of the blood, and the increased rouleaux formation of red cells. Increased sedimentation rate of red cells of the blood occurs when there is increased amount of fibrinogen in the plasma. Fibrinogen is formed principally in the liver, and the plasma normally contains 180 to 400mg. fibrinogen per 100ml. .When fibrinogen concentration falls to 60mg. or less per 100ml. haemorrhage occur. Acquired Fibrinogenopenia may occur in severe liver disease, amyloidosis, malignancy, tuberculosis and many other conditions. Congenital Fibrinogenopenia has been reported in which fibrinogen is either completely absent or greatly reduced. In both type, some diminution of platelets also exist, which is responsible positive tourniquet test and increased bleeding time, patients with no fibrinogen have their blood completely incoagulable; most of them die of blood loss in childhood. Diagnosis : coagulation time prolonged, prothrombin time prolonged, bleeding time frequently prolonged. Fibrinogen coagulates at 580 C; so , if plasma is heated to 600 C and remains clear, the inference is that no fibrinogen is present in plasma. By this test, haemophilia an be differentiated from coagulation defect due to Fibrinogenopenia.
Fibrinolysis causes significant reduction in fibrinogen content of blood. This is found to occur on the first day of menstruation, in some toxaemias of pregnancy, after I.V. typhoid vaccine or mercurial diuretics, in severe shocks due to extensive haemorrhage or burns. It is believed that all these conditions release tissue enzymes capable of activating the fibrinolysin of plasma. Premature separation of placenta is specially liable to cause fibrinogen preparations are injected. Again in these conditions, hypoprothrombinaemia may accompany the Fibrinogenopenia as will be evident from prolonged prothrombin time.

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