Platelets

Fig

Hemostasis the process by which the bleeding is stopped from broken vessels. steps involved: Vascular spasm. Platelets plug formation. Blood coagulation Clot retraction Fibrinolysis

Vascular spasm

PLATELETS PLUG FORMATION The role of ADP, Thromboxane A2 in plug formation. The role of prostacyclin. The process begins with activation of platelets by their contact with collagen fibers at the tissue level. activated platelets play also roles in vascular reaction and coagulation.

Fig

Hemostasis the process by which the bleeding is stopped from broken vessels. steps involved: Vascular spasm. Platelets plug formation. Blood coagulation (Clotting) Clot retraction Fibrinolysis

Coagulation Factors

FibrinogenFibrin Thrombin Prothrombin Xa Va VIIa TF Extrinsic Pathway IXa VIIIa XIa XIIa Intrinsic pathway XIIIa Soft clot Fibrin Hard clot V VIII

Fig

Hemostasis the process by which the bleeding is stopped from broken vessels. steps involved: Vascular spasm. Platelets plug formation. Blood coagulation (Clotting) Clot retraction Fibrinolysis

Plasminogen  Plasmin  fibrinolysis.  Thrombin, factor XII, tissue plasminogen activators

Control mechanisms of hemostasis - Prostacyclin opposes platelets adhesion (the action of thromboxane A2). - Antithrombin III: blocks the action of XII, XI, IX, X and II. - Protein C: inactivates factors V and VIII. Enhances the activity of plasminogen activators. - Alpha-1- antitrypsin: inhibits factor XI. - Heparin: increases effectiveness of antithrombin III.

Bleeding Disorders

Causes of Bleeding disorders Vascular defects: Thrombocyte defects: Disorders of coagulation factors:

Causes of Bleeding and coagulation disorders Vascular defects: Thrombocyte defects: Thrombocytosis: -Primary = myeloproliferative disorders = polycythemia vera and some types of leukemias. - Secondary: due to temporarily underlying cause : stress, exercise  release from storage pool. Hemorrhage or hemolytic anemia  increased production. Removal of spleen  decrease destruction. Causes an increase over 1,000,000/mm3. This results in increased aggregation  thrombosis of small vessels. Disorders of coagulation factors:

Thrombocyte disorders Vascular defects: Thrombocyte defects: –Thrombocytopenia: (count below 100,000/mm3). * Causes: Decreased production or increased destruction. *Symptoms and signs: - Ecchymosis and petechiae (when fall below 30,000/mm3) - Increased bleeding time. Disorders of coagulation factors:

Thrombocytopenia: Causes - Decreased production: Myelofibrosis, aplastic anemia, metastasis, chemotherapy, Deficiency of B12 and folate. - Excessive destruction of platelets: conditions that cause splenomegaly (hepatic cirrhosis, lymphomas and myeloproliferative diseases. (spleen holds one third of platelets). Drugs: quinidine, gold, and autoantibodies in autoimmune diseases (LE (Lupus Erythematosus), chronic lymphocytic leukemia, idiopathic thrombocytopenic purpura).

Thrombocytopathy: Drugs (aspirin, indomethacine, phenylbutazone inhibit aggregation). Diseases: plasma proteins (in macroglobulinemia, multiple myeloma) may interfere with platelets function, and fibrin polymerization.

Coagulation Factors Vascular defects: Thrombocyte defects: Disorders of coagulation factors: Inhereted: -Hemophilia: X linked recessive disease. A= deficient or absent factor VIII. B = deficient or absent factor IX. (Christmas disease). PTT is prolonged and PT is normal, bleeding time is normal -Von Willebrand’s disease = PTT and bleeding time prolonged ( platelet adhesion defect). Treatment: Adm. of factors Teaching patient and families safety measures.

Coagulation Factors Vascular defects: Thrombocyte defects: Disorders of coagulation factors: Acquired: By decreased production or increased consumption - Decreased production: - Vit K deficiency (II, VII, IX, and X) Malabsorption, malnutrition, or GI sterilization with Antibiotics. Treatment: replacement of factors by giving fresh plasma and Vit. K. - liver diseases ( II, V, VII, IX, and X) PT, and PTT are prolonged.

Blood tests for Bleeding disorders Bleeding time. PT = prothrombin time (extrinsic pathway). PTT = Partial thromboplastin time = intrinsic pathway. (60-90sec) phospholipid is added to citrated plasma. APTT = activated partial thromboplastin time = adding contact activating agent kaolin ( reduces time to 26-42sec. Thrombin clotting time (TT)= thrombin is added (10-13 sec).detects the final stage of transformation of fibrinogen to fibrin

Blood Groups

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Hemolysis of Red Blood Cells Blood Transfusion Erythroblastosis fetalis

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GOOD LUCK