Bleeding and thrombosis

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Splenic artery embolization in a woman with bleeding gastric varices and splenic vein thrombosis: a case report...

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Clinical Presentation Symptoms The clinical onset of the chronic phase is generally insidious. Accordingly, some patients are diagnosed while still asymptomatic, during health-screening tests; other patients present with fatigue, malaise, and weight loss or have symptoms resulting from splenic enlargement, such as early satiety and left upper quadrant pain or mass. Less common are features related to granulocyte or platelet dysfunction, such as infections, thrombosis, or bleeding.

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Mixing Studies Mixing studies are used to evaluate a prolonged aPTT or, less commonly PT, to distinguish between a factor deficiency and an inhibitor. In this assay, normal plasma and patient plasma are mixed in a 50:50 ratio, and the aPTT or PT is determined immediately and after incubation at 37oC for varying times, typically 30, 60, and/or 120 min. With isolated factor deficiencies, the aPTT will correct with mixing and stay corrected with incubation. With aPTT prolongation due to a lupus anticoagulant, the mixing and incubation will show no correction.

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Screening Assays The most commonly used screening tests are the PT, aPTT, and platelet count. The PT assesses the factors I (fibrinogen), II (prothrombin), V, VII and X (Fig. 59-6). The PT measures the time for clot formation of the citrated plasma after recalcification and addition of thromboplastin, a mixture of TF and phospholipids. The sensitivity of the assay varies by the source of thromboplastin.

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The most important point in a history related to venous thrombosis is whether the thrombotic event was idiopathic (meaning there was no clear precipitating factor) or was a precipitated event. In patients without underlying malignancy, having an idiopathic event is the strongest predictor of recurrence of venous thromboembolism. In patients who have a vague history of thrombosis, a history of being treated with warfarin suggests a past DVT.

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Underlying Systemic Diseases that Cause or Exacerbate a Bleeding Tendency Acquired bleeding disorders are commonly secondary to, or associated with, systemic disease. The clinical evaluation of a patient with a bleeding tendency must therefore include a thorough assessment for evidence of underlying disease. Bruising or mucosal bleeding may be the presenting complaint in liver disease, severe renal impairment, hypothyroidism, paraproteinemias or amyloidosis, and conditions causing bone marrow failure.

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Epistaxis is a common symptom, particularly in children and in dry climates, and may not reflect an underlying bleeding disorder. However, it is the most common symptom in hereditary hemorrhagic telangiectasia and in boys with vWD. Clues that epistaxis is a symptom of an underlying bleeding disorder include lack of seasonal variation and bleeding that requires medical evaluation or treatment, including cauterization. Bleeding with eruption of primary teeth is seen in children with more severe bleeding disorders, such as moderate and severe hemophilia.

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Sites of action of the four major physiologic antithrombotic pathways: antithrombin (AT); protein C/S (PC/PS); tissue factor pathway inhibitor (TFPI); and the fibrinolytic system, consisting of plasminogen, plasminogen activator (PA), and plasmin. PT, prothrombin; Th, thrombin; FDP, fibrin(ogen) degradation products. [Modified from BA Konkle, AI Schafer, in DP Zipes et al (eds): Braunwald's Heart Disease, 7th ed. Philadelphia, Saunders, 2005.] Antithrombin (or antithrombin III) is the major plasma protease inhibitor of thrombin and the other clotting factors in coagulation.

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Approach to the Patient: Bleeding and Thrombosis Clinical Presentation Disorders of hemostasis may be either inherited or acquired. A detailed personal and family history is key in determining the chronicity of symptoms and the likelihood of the disorder being inherited and it provides clues to underlying conditions that have contributed to the bleeding or thrombotic state.

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Coagulation is initiated by tissue factor (TF) exposure, which, with factor (F)VIIa, activates FIX and FX, which in turn, with FVIII and FV as cofactors, respectively, results in thrombin formation and subsequent conversion of fibrinogen to fibrin. Thrombin activates FXI, FVIII, and FV, amplifying the coagulation signal. Once the TF/FVIIa/FXa complex is formed, tissue factor pathway inhibitor (TFPI) inhibits the TF/FVIIa pathway, making coagulation dependent on the amplification loop through FIX/FVIII.

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Harrison's Internal Medicine Chapter 59. Bleeding and Thrombosis Bleeding and Thrombosis: Introduction The human hemostatic system provides a natural balance between procoagulant and anticoagulant forces. The procoagulant forces include platelet adhesion and aggregation and fibrin clot formation; anticoagulant forces include the natural inhibitors of coagulation and fibrinolysis. Under normal circumstances, hemostasis is regulated to promote blood flow; however, it is also prepared to clot blood rapidly to arrest blood flow and prevent exsanguination.

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