COAGULAZIONE INTRAVASCOLARE DISSEMINATA PDF

Rischio di coagulazione intravascolare disseminata in pazienti sottoposti ad agobiopsia prostatica transperineale ecoguidata con sonda transrettale. Primary . L’insieme delle alterazioni dell’emostasi, che siano congenite come le emofilie o acquisite come le coagulazioni intravascolari disseminate (CID), richiede una. coagulazione coagulazione del sangue coagulazione intravascolare colelita coagulazione intravascolare disseminata coagulo.

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We think you have liked this presentation. If you wish to download it, please recommend it to your friends in any social system. Share buttons are a little bit lower. Published by Alejandro Stevenson Modified over 4 years ago. There are three main types of VWD. Type I – by far the most common form. Inheritance is autosomal dominant. Most patients are heterozygotes. Mild to moderate decrease in plasma VWF concentrations. Most patients have mild disease with excessive bleeding after surgery or trauma.

IIa – deficiency in high and medium molecular weight VWF due to either inability to secrete them from the megakaryocyte or endothelial cell or due to proteolysis as soon as they enter the circulation.

Most individuals are the offspring of inrravascolare Type I patients and dissemonata homozygous. Perioperatively, either must intraascolare given twice a day until hours post-op 2.

Effects last days before tachyphylaxis can occur 3. Aspirin is totally contraindicated in patients with VWD because of inhibitory effect on platelet aggegration. This would exacerbate VWD. Most common inherited bleeding disorder B.

Mild bleeding disorder often undiagnosed C. Autosomal dominant disorder II. Von Willebrand factor mediates platelet adhesion B. Symptoms and Signs A. Severe Menorrhagia common presentation in women B. Postpartum Hemorrhage several days after delivery IV. Lab Results vary over time in each patient B.

Bleeding Time prolonged V. Indicated for surgery or trauma B. When activated, it becomes a trimer which has lost most of the B domain. Inheritance is X-linked recessive. Incidence is 1 in live male births. Suspect hemophilia in any male who has history of extensive bleeding after trauma or spontaneous bleeding into joints and muscles. Excessive bleeding at time of circumcision 3. Prolongation of aPTT variable with degree of hemophilia 2. Normal vonWillebrand Factor and Ristocetin cofactor 4.

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Antifibrinolytics such as aminocaproic acid may be helpful. Acquired, not inherited B. Inhibitors can also occur in non-hemophiliac patients in the setting of: Idiopathic conditions – i. Autoimmune disorders such as systemic lupus erythematosus, rheumatoid arthritis, etc.

Malignancies such as lymphoproliferative disorders, lymphomas, and solid tumors.

Drug reactions to penicillin, chloramphenicol, phenytoin, etc. Pregnancy and the postpartum state. Risk factors for development of antibodies 1. Patients with severe hemophilia are at much higher risk because intravascolars are exposed to more FVIII therapy. These patients are at greater risk for developing antibodies after treatment with FVIII concentrates. There are two main types of antibodies Type I antibodies – seen in classic intravascolate. Type II antibodies – these are the autoantibodies and they exhibit a more complex pattern of inhibition.

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Acquired inhibitors should be suspected when non-hemophiliac patients present with spontaneous hematomas with sudden, life-threatening bleeds. However, the presence coagulazlone FVIII inhibitor can be confirmed by adding inhibitor plasma with normal plasma and then assaying all the residual clotting factors in the normal plasma. Quantification of the inhibitor can be done with the Bethesda Assay.

Characteristics of patients – Grouped as low responders or high responders 1. Low responders are patients who usually have low titers of inhibitor less than 10 BUwhich does not increase after challenge with FVIII. Therefore, these patients do not show significant anamnestic response with subsequent FVIII treatments. High responders are mostly hemophiliacs who develop a high titer of inhibitor when challenged with FVIII. Mild bleeding episodes – options include: Management Low responders a.

However, these two are under clinical trials currently and may be associated with increased risk of thrombosis. Severe bleeding – options include: Mild bleeding episodes – considerations include: Avoiding FVIII products to prevent an anamnestic response, which would preclude this treatment from being a treatment option in the event of future bleeding episodes.

Severe bleeding episodes Use human or porcine FVIII until an anamnestic response occurs, after which a bypass agent must be used instead. Immunosuppressive agents to control antibody production Corticosteroids Cyclophosphamide Azithoprine b. Intravenous gamma globulin – in the hope that some antibodies in this pooled sample may be directed against the inhibitor c.

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Induction of immune tolerance to suppress inhibitor formation by administration of FVIII on a continuous basis.

FIXa is a serine protease.

Hemophilia B Christmas Disease A. Incidence is 1 in 30, live male births. Mechanism – quantitative deficiency in the synthesis of FIX.

Clinical features – identical to Hemophilia A 1. Suspect hemophilia in any male who has history of extensive bleeding after trauma or spontaneous bleeding into joints or muscles. Bleeding at time of circumcision 3. Decreased FIX acitvity 3.

Normal bleeding time and thrombin time. Mild hemophilia – Antifibrinolytics such as aminocaproic acid may be helpful. For major surgery, give FIX concentrates perioperatively. Higher levels may lead to thrombosis see below. Moderate and Severe hemophilia – give FIX concentrate at the earliest sign of bleeding. Fresh frozen plasma – contains FIX. Limited by the fact that unless exchange transfusion is done, sufficient FFP cannot be given to patients with severe hemophilia to raise FIX levels sufficiently in order to prevent or control bleeding episodes.

Amniotic Fluid Embolism 3. Retained fetal products 4. Immune complex disorders 2. Incompatible blood transfusion 4. Cyanotic Congenital Heart Disease 4. Deficit vitamina C D. Malattie del collagene vasculiti E.

Paraproteinemia amiloidosi, crioglobulinemia F. Telangectasia emorragica ereditaria G. Drug induced Thrombocytopenia heparin 2. Autoimmune Hemolytic Anemia 5. Prosthetic heart valves 2. Hemorrhage with extensive transfusion 7.

Suppression of Megakaryocytes Acquired Hereditary a.

Schistocita – Wikipedia

Thrombocytopenia-absent radii TAR syndrome 2. Wiskott-Aldrich syndrome x-linked condition 4.

Defects of platelet aggregation Thrombasthenia Glanzmann’s disease Acquired defects: Inheritance – autosomal dominant B. Mean onset of DVT: Increased risk of venous thrombosis and pulmonary embolism. Venous thrombosis occurs most frequently in the deep veins of the lower extremities.