Hemostasis & Blood Disorders

olanjones's version from 2017-02-22 23:12

Values & Components

Question Answer
What is the normal range for RBCs4.5-6.2 million/mcL (live 120 days)
What is the normal range for hemoglobin?Women = 12-16 g/dL, Men = 14-18 g/dL
What is the normal range for hematocrit?37-52% (think 3x hgb)
What is the normal range for WBC?4,000-10,000
What is the normal range for platelets?150,000-340,000 (live 8-12 days)
What is erythropoietin and where is it produced?hormone that stimulate RBC production, is produced in the kidney
What is thrombopoietin and where is it produced?hormone that stimulates platelet production, is produced in liver, kidney, smooth muscle, bone marrow
Where are the clotting factors synthesized?in the liver, therefore liver damage decreases ability to clot (requires Vitamin K)
What is Hemophilia A?a disease is a genetic lack of Factor VIII
What is von Willebrand disease?a hereditary disease in which one lacks von Willebrand factor - MOST COMMON HEREDITARY BLEEDING DISORDER
What is the function of von Willebrand factor?causes "stickiness" of collagen to allow platelets to aggregate


Question Answer
What is primary hemostasis?Reflex vasoconstriction to prevent blood loss, vWF is stimulated by damaged endothelial cells and binds with collagen allowing platelets to adhere, activated platelets release TXA2 and ADP to attract more platelets
What is secondary hemostasis?the clotting cascade, clot retraction, clot dissolution
Common pathway of the Clotting cascadeFactor X + Calcium = Factor Xa + Calcium cleaves Prothrombin to produce Thrombin triggers Fibrinogen + Calcium > Fibrin (monomer) > Fibrin (polymer)
Extrinsic pathway of the Clotting cascadeFactor VII + Calcium produces Factor VIIa which with Calcium triggers the common pathway (faster pathway than intrinsic)
Intrinsic pathway of Clotting cascadeFactor XII > Factor XIIa > Factor XI > Factor XIa > Factor IX + Calcium > Factor IXa which with Factor VIIIa and Calcium triggers the common pathway
How does clot retraction occur?the actin and myosin of the platelets contract to pull the fibrin tighter around the platelets
What causes clot dissolution?tissue plasminogen activator (tPA = clot buster!) cleaves plasminogen to form plasmin, plasmin digests the fibrin
What blood test is used to evaluate the extrinsic pathway?PT/INR (prothrombin time/international normalized ratio), also used to monitor Coumadin effect
What blood test is used to evaluate the intrinsic pathway?PTT (partial thromboplastin time), also used to monitor Heparin effects


Question Answer
What are the two types of absolute polycythemia (increased production of RBC)?Primary: due to red cell precursors, often includes increase in all blood cells. Secondary: due to increased production of erythropoietin in response to hypoxia
What is relative polycythemia?an increased hematocrit level due to increased concentration, secondary to dehydration
What are the physiological effects of polycythemia?increased viscosity, decrease in blood flow, increased risk of clot/obstruction, can result in clot formation and ischemic conditions. Ruddy complexion, HA, backache, fatigue
What is thrombocytopenia and its causes?platelet level less than 150,000. Caused by bone marrow suppression, cancer, viral infection, accelerated destruction of platelets
What are the physiological effects of thrombocytopeina?increased bleeding (cannot clot), can result in petechiae, purpura, gingival bleeding
What is Immune Thrombocytic Purpura (ITP)?an autoimmune disorder often following a bacterial or viral infection. Platelets are tagged for destruction (in the spleen) by the immune system


Question Answer
What can cause disseminated intravascular coagulation (DIC)?Trauma, Sepsis, Cancer. Tissue factor release leads to massive act of the clotting cascade
Why is DIC especially deadly?platelet stores and clotting factors are exhausted so hemostasis cannot be achieved, fibrinolysis is also activated inhibiting thrombin and platelet aggregation (leads to bleeding), fibrin is deposited intravascularly leading to thrombosis production, hemolytic anemia, and tissue ischemia
How is DIC treated? replace platelets, RBCs, heparin therapy (controversial)

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