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Streptokinase is a thrombolytic medication activating plasminogen by nonenzymatic mechanism. [1] As a medication it is used to break down clots in some cases of myocardial infarction (heart attack), pulmonary embolism, and arterial thromboembolism. [2] The type of heart attack it is used in is an ST elevation myocardial infarction (STEMI). [3]
Streptococcus canis is a group G beta-hemolytic species of Streptococcus. [1] It was first isolated in dogs, giving the bacterium its name. These bacteria are characteristically different from Streptococcus dysgalactiae, which is a human-specific group G species that has a different phenotypic chemical composition.
However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems. Tissue plasminogen activator (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen. [14] This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme, plasmin. [15]
Tissue-type plasminogen activator, short name tPA, is a protein that facilitates the breakdown of blood clots. It acts as an enzyme to convert plasminogen into its active form plasmin, the major enzyme responsible for clot breakdown.
The treatments to prevent the formation of blood clots is balanced against the risk of bleeding. [5] One of the goals of blood clot prevention is to limit venous stasis as this is a significant risk factor for forming blood clots in the deep veins of the legs. [6] Venous stasis can occur during the long periods of not moving.
In addition, pathogenic bacteria may secrete agents that alter the coagulation system, e.g. coagulase and streptokinase. [39] Immunohemostasis is the integration of immune activation into adaptive clot formation. Immunothrombosis is the pathological result of crosstalk between immunity, inflammation, and coagulation.
Fibrinolysis (simplified). Blue arrows denote stimulation, and red arrows inhibition. Plasmin is a serine protease that acts to dissolve fibrin blood clots. Apart from fibrinolysis, plasmin proteolyses proteins in various other systems: It activates collagenases, some mediators of the complement system, and weakens the wall of the Graafian follicle, leading to ovulation.
Thromboangiitis obliterans, also known as Buerger disease (English / ˈ b ɜːr ɡ ər /; German: [ˈbʏʁɡɐ]) or Winiwarter-Buerger disease, is a recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet.