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Questions and Answers
What is primary thrombocytosis characterized by?
What is primary thrombocytosis characterized by?
What is secondary thrombocytosis characterized by?
What is secondary thrombocytosis characterized by?
What is thrombocytopenia characterized by?
What is thrombocytopenia characterized by?
What are common platelet disorders?
What are common platelet disorders?
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What are hereditary platelet function disorders?
What are hereditary platelet function disorders?
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What is Hemophilia A?
What is Hemophilia A?
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What are laboratory studies for Hemophilia A?
What are laboratory studies for Hemophilia A?
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What is Von Willebrand disease?
What is Von Willebrand disease?
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What are laboratory studies for DIC?
What are laboratory studies for DIC?
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What are acquired platelet function disorders?
What are acquired platelet function disorders?
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What is the cause of primary thrombocytosis?
What is the cause of primary thrombocytosis?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What is primary thrombocytosis characterized by?
What is primary thrombocytosis characterized by?
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What is secondary thrombocytosis characterized by?
What is secondary thrombocytosis characterized by?
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What is thrombocytopenia characterized by?
What is thrombocytopenia characterized by?
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What are common platelet disorders?
What are common platelet disorders?
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What are hereditary platelet function disorders?
What are hereditary platelet function disorders?
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What is Hemophilia A?
What is Hemophilia A?
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What are laboratory studies for Hemophilia A?
What are laboratory studies for Hemophilia A?
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What is Von Willebrand disease?
What is Von Willebrand disease?
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What are laboratory studies for DIC?
What are laboratory studies for DIC?
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What are acquired platelet function disorders?
What are acquired platelet function disorders?
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What is the cause of primary thrombocytosis?
What is the cause of primary thrombocytosis?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What is the most common cause of thrombocytopenia?
What is the most common cause of thrombocytopenia?
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Which of the following is NOT a hereditary platelet function disorder?
Which of the following is NOT a hereditary platelet function disorder?
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What is the most common cause of primary thrombocytosis?
What is the most common cause of primary thrombocytosis?
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Which of the following is NOT a clinical feature of Von Willebrand disease?
Which of the following is NOT a clinical feature of Von Willebrand disease?
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What is the treatment for Hemophilia A?
What is the treatment for Hemophilia A?
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Which of the following is NOT an acquired platelet function disorder?
Which of the following is NOT an acquired platelet function disorder?
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What are laboratory studies for DIC?
What are laboratory studies for DIC?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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Which of the following is NOT a cause of common platelet disorders?
Which of the following is NOT a cause of common platelet disorders?
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What is the most common cause of secondary thrombocytosis?
What is the most common cause of secondary thrombocytosis?
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Which of the following is NOT a clinical feature of primary thrombocytosis?
Which of the following is NOT a clinical feature of primary thrombocytosis?
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What is the characteristic laboratory finding in Hemophilia A?
What is the characteristic laboratory finding in Hemophilia A?
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What is primary thrombocytosis?
What is primary thrombocytosis?
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What is secondary thrombocytosis?
What is secondary thrombocytosis?
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What platelet count is associated with primary thrombocytosis?
What platelet count is associated with primary thrombocytosis?
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What is thrombocytopenia?
What is thrombocytopenia?
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What is Hemophilia A?
What is Hemophilia A?
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What are laboratory studies for Hemophilia A?
What are laboratory studies for Hemophilia A?
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What is Von Willebrand disease?
What is Von Willebrand disease?
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What are laboratory studies for DIC?
What are laboratory studies for DIC?
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What are acquired platelet function disorders?
What are acquired platelet function disorders?
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What are common platelet disorders?
What are common platelet disorders?
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What are hereditary platelet function disorders?
What are hereditary platelet function disorders?
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What is the cause of acquired coagulopathies?
What is the cause of acquired coagulopathies?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What is the most common cause of secondary thrombocytosis?
What is the most common cause of secondary thrombocytosis?
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What is the most common cause of decreased platelet production?
What is the most common cause of decreased platelet production?
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What is the deficiency in hereditary platelet function disorder GPIIb?
What is the deficiency in hereditary platelet function disorder GPIIb?
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What is the treatment for Hemophilia A?
What is the treatment for Hemophilia A?
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What are the clinical features of Von Willebrand disease?
What are the clinical features of Von Willebrand disease?
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What are the laboratory studies for acquired coagulopathies?
What are the laboratory studies for acquired coagulopathies?
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What is the most common cause of acquired platelet function disorders?
What is the most common cause of acquired platelet function disorders?
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What is the most common cause of thrombocytopenia?
What is the most common cause of thrombocytopenia?
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What is the laboratory finding in Hemophilia A?
What is the laboratory finding in Hemophilia A?
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What is the most common cause of acquired coagulopathies?
What is the most common cause of acquired coagulopathies?
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What is the cause of primary thrombocytosis?
What is the cause of primary thrombocytosis?
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What is primary thrombocytosis characterized by?
What is primary thrombocytosis characterized by?
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What is secondary thrombocytosis characterized by?
What is secondary thrombocytosis characterized by?
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What is thrombocytopenia characterized by?
What is thrombocytopenia characterized by?
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What are common platelet disorders?
What are common platelet disorders?
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What are hereditary platelet function disorders?
What are hereditary platelet function disorders?
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What is Hemophilia A?
What is Hemophilia A?
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What are laboratory studies for Hemophilia A?
What are laboratory studies for Hemophilia A?
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What is Von Willebrand disease?
What is Von Willebrand disease?
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What are laboratory studies for DIC?
What are laboratory studies for DIC?
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What are acquired platelet function disorders?
What are acquired platelet function disorders?
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What causes secondary thrombocytosis?
What causes secondary thrombocytosis?
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What is the difference between primary and secondary thrombocytosis?
What is the difference between primary and secondary thrombocytosis?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What is the cause of secondary thrombocytosis?
What is the cause of secondary thrombocytosis?
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What is the most common cause of decreased platelet production?
What is the most common cause of decreased platelet production?
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What is the most common cause of increased platelet destruction?
What is the most common cause of increased platelet destruction?
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What are the three types of hereditary platelet function disorders?
What are the three types of hereditary platelet function disorders?
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What is the laboratory finding for Hemophilia A?
What is the laboratory finding for Hemophilia A?
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What is the treatment for Hemophilia A?
What is the treatment for Hemophilia A?
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What is the inheritance pattern of Von Willebrand disease?
What is the inheritance pattern of Von Willebrand disease?
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What are the clinical features of Von Willebrand disease?
What are the clinical features of Von Willebrand disease?
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What are the laboratory findings for DIC?
What are the laboratory findings for DIC?
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What is the cause of acquired platelet function disorders?
What is the cause of acquired platelet function disorders?
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What is the cause of Hemophilia A?
What is the cause of Hemophilia A?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What is the cause of Hemophilia A?
What is the cause of Hemophilia A?
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What is the most common clinical presentation of Von Willebrand disease?
What is the most common clinical presentation of Von Willebrand disease?
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What is the laboratory finding in DIC?
What is the laboratory finding in DIC?
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What is the characteristic feature of secondary thrombocytosis?
What is the characteristic feature of secondary thrombocytosis?
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What is the cause of acquired platelet function disorders?
What is the cause of acquired platelet function disorders?
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What is the clinical presentation of primary thrombocytosis?
What is the clinical presentation of primary thrombocytosis?
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What is the laboratory finding in Hemophilia A?
What is the laboratory finding in Hemophilia A?
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What is the characteristic feature of thrombocytopenia?
What is the characteristic feature of thrombocytopenia?
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What is the cause of Von Willebrand disease?
What is the cause of Von Willebrand disease?
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What is the characteristic feature of hereditary platelet function disorders?
What is the characteristic feature of hereditary platelet function disorders?
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What is the cause of secondary thrombocytosis?
What is the cause of secondary thrombocytosis?
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Platelets are produced by the liver.
Platelets are produced by the liver.
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Primary thrombocytosis is a benign condition.
Primary thrombocytosis is a benign condition.
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Platelet counts can be >1000 X 10 /L in primary thrombocytosis.
Platelet counts can be >1000 X 10 /L in primary thrombocytosis.
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Secondary thrombocytosis is usually in response to thrombopoietin.
Secondary thrombocytosis is usually in response to thrombopoietin.
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Thrombocytopenia can result in abnormal bleeding associated with thrombocytopenia.
Thrombocytopenia can result in abnormal bleeding associated with thrombocytopenia.
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Hereditary platelet function disorders include deficiency of membrane GPIIb.
Hereditary platelet function disorders include deficiency of membrane GPIIb.
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Acquired platelet function disorders include only antiplatelet drugs.
Acquired platelet function disorders include only antiplatelet drugs.
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Hemophilia A predominately affects females.
Hemophilia A predominately affects females.
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Hemophilia A laboratory studies show prolonged PT and normal PTT.
Hemophilia A laboratory studies show prolonged PT and normal PTT.
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Von Willebrand disease is a bleeding disorder associated with excessive clotting.
Von Willebrand disease is a bleeding disorder associated with excessive clotting.
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Acquired coagulopathies include vitamin K deficiency and liver disease.
Acquired coagulopathies include vitamin K deficiency and liver disease.
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DIC causes widespread microthrombi with elevated fibrinogen.
DIC causes widespread microthrombi with elevated fibrinogen.
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Platelets are produced by the fragmentation of megakaryocyte nuclei in the bone marrow.
Platelets are produced by the fragmentation of megakaryocyte nuclei in the bone marrow.
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Primary thrombocytosis is a controlled, non-malignant proliferation of platelets in response to thrombopoietin.
Primary thrombocytosis is a controlled, non-malignant proliferation of platelets in response to thrombopoietin.
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Secondary thrombocytosis is usually a response to thrombopoietin and is characterized by elevated platelet counts.
Secondary thrombocytosis is usually a response to thrombopoietin and is characterized by elevated platelet counts.
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Thrombocytopenia is characterized by a platelet count above 100 x 10^9/L.
Thrombocytopenia is characterized by a platelet count above 100 x 10^9/L.
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Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α granules or dense granules.
Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α granules or dense granules.
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Acquired platelet function disorders include hyperglobulinemia associated with multiple myeloma.
Acquired platelet function disorders include hyperglobulinemia associated with multiple myeloma.
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Hemophilia A is an autosomal dominant condition resulting from a deficiency of factor VIII.
Hemophilia A is an autosomal dominant condition resulting from a deficiency of factor VIII.
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Hemophilia A predominately affects females.
Hemophilia A predominately affects females.
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Von Willebrand disease is an autosomal recessive bleeding disorder.
Von Willebrand disease is an autosomal recessive bleeding disorder.
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Acquired coagulopathies include vitamin K deficiency and liver disease.
Acquired coagulopathies include vitamin K deficiency and liver disease.
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DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage.
DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage.
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The laboratory studies for Hemophilia A show a prolonged PT and normal PTT.
The laboratory studies for Hemophilia A show a prolonged PT and normal PTT.
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Platelets are produced by fragmentation of megakaryocyte cytoplasm in the liver.
Platelets are produced by fragmentation of megakaryocyte cytoplasm in the liver.
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Primary thrombocytosis is a controlled, malignant proliferation of platelets in response to thrombopoietin.
Primary thrombocytosis is a controlled, malignant proliferation of platelets in response to thrombopoietin.
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Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
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Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
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Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
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Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
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Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
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Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
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Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
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Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
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Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
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Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
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What is the process by which platelets are produced?
What is the process by which platelets are produced?
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What is primary thrombocytosis and what can cause it?
What is primary thrombocytosis and what can cause it?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What are the complications associated with primary thrombocytosis?
What are the complications associated with primary thrombocytosis?
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What is secondary thrombocytosis and how is it characterized?
What is secondary thrombocytosis and how is it characterized?
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What is thrombocytopenia and what can cause it?
What is thrombocytopenia and what can cause it?
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What are hereditary platelet function disorders and what are some examples?
What are hereditary platelet function disorders and what are some examples?
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What are acquired platelet function disorders and what can cause them?
What are acquired platelet function disorders and what can cause them?
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What is Hemophilia A and what causes it?
What is Hemophilia A and what causes it?
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What are the clinical features of Von Willebrand disease?
What are the clinical features of Von Willebrand disease?
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What are laboratory studies used to diagnose Hemophilia A?
What are laboratory studies used to diagnose Hemophilia A?
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What are laboratory studies used to diagnose DIC?
What are laboratory studies used to diagnose DIC?
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What is the difference between primary and secondary thrombocytosis?
What is the difference between primary and secondary thrombocytosis?
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What are some common platelet disorders?
What are some common platelet disorders?
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What are some hereditary platelet function disorders?
What are some hereditary platelet function disorders?
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What is Hemophilia A and what are its symptoms?
What is Hemophilia A and what are its symptoms?
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What are the laboratory studies for Hemophilia A?
What are the laboratory studies for Hemophilia A?
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What is Von Willebrand disease and what are its clinical features?
What is Von Willebrand disease and what are its clinical features?
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What is DIC and what are its laboratory findings?
What is DIC and what are its laboratory findings?
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What causes primary thrombocytosis?
What causes primary thrombocytosis?
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What is the platelet count associated with primary thrombocytosis?
What is the platelet count associated with primary thrombocytosis?
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What are acquired platelet function disorders?
What are acquired platelet function disorders?
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What is the difference between primary and secondary hemostasis?
What is the difference between primary and secondary hemostasis?
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What is the role of von Willebrand factor in hemostasis?
What is the role of von Willebrand factor in hemostasis?
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- ____________ is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- ____________ is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
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- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the ____________ marrow.
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the ____________ marrow.
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- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet ____________.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet ____________.
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- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or ____________ granules.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or ____________ granules.
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- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in ____________ failure.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in ____________ failure.
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- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of ____________.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of ____________.
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- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII ____________.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII ____________.
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- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and ____________ in young females.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and ____________ in young females.
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- Acquired coagulopathies include vitamin K deficiency and ____________ disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
- Acquired coagulopathies include vitamin K deficiency and ____________ disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
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- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or ____________ complications.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or ____________ complications.
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-______Secondary______thrombocytosis______is______characterized______by______increased______platelet______production,______usually______in______response______to______thrombopoietin,______and______platelet______count______is______elevated,but______usually<1000______X______10/L.
-______Secondary______thrombocytosis______is______characterized______by______increased______platelet______production,______usually______in______response______to______thrombopoietin,______and______platelet______count______is______elevated,but______usually<1000______X______10/L.
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- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or ____________.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or ____________.
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- Platelets are produced by fragmentation of ______ cytoplasm in the bone marrow.
- Platelets are produced by fragmentation of ______ cytoplasm in the bone marrow.
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- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
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- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or ______ complications.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or ______ complications.
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- Secondary thrombocytosis is characterized by increased platelet ______ usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Secondary thrombocytosis is characterized by increased platelet ______ usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
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- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet ______.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet ______.
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- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or ______.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or ______.
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- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or ______ granules.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or ______ granules.
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- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and ______ in renal failure.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and ______ in renal failure.
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- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of ______.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of ______.
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- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and ______ in young females.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and ______ in young females.
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- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (______).
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (______).
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- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is ______ concentrate.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is ______ concentrate.
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What is the process that involves the removal of fibrin and is initiated when clotting begins?
What is the process that involves the removal of fibrin and is initiated when clotting begins?
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Which of the following is NOT a group of coagulation proteins?
Which of the following is NOT a group of coagulation proteins?
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Which group of coagulation factors contains vitamin K dependent coagulation factors II, VII, IX, and X?
Which group of coagulation factors contains vitamin K dependent coagulation factors II, VII, IX, and X?
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Which group of coagulation factors is involved in the initial activation of the intrinsic pathway and fibrinolysis?
Which group of coagulation factors is involved in the initial activation of the intrinsic pathway and fibrinolysis?
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What is the process that involves the formation of an unstable platelet plug?
What is the process that involves the formation of an unstable platelet plug?
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What is the process that involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
What is the process that involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
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What are the three indices used to classify anemia based on erythrocyte size and hemoglobin content?
What are the three indices used to classify anemia based on erythrocyte size and hemoglobin content?
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Where do most coagulation reactions occur?
Where do most coagulation reactions occur?
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What are the two stages of hemostasis?
What are the two stages of hemostasis?
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What are the coagulation mechanisms involved in?
What are the coagulation mechanisms involved in?
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Which group of coagulation factors contains coagulation factors I, V, VIII, and XIII?
Which group of coagulation factors contains coagulation factors I, V, VIII, and XIII?
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What do erythrocyte indices help classify erythrocytes based on?
What do erythrocyte indices help classify erythrocytes based on?
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Which type of hemostasis involves the formation of an unstable platelet plug?
Which type of hemostasis involves the formation of an unstable platelet plug?
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Which type of hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
Which type of hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
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Which group of coagulation proteins contains vitamin K dependent coagulation factors II, VII, IX, and X?
Which group of coagulation proteins contains vitamin K dependent coagulation factors II, VII, IX, and X?
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Which group of coagulation proteins contains coagulation factors I, V, VIII, and XIII?
Which group of coagulation proteins contains coagulation factors I, V, VIII, and XIII?
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Which group of coagulation proteins includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis?
Which group of coagulation proteins includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis?
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Where do most coagulation reactions occur?
Where do most coagulation reactions occur?
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What is the process of removing fibrin called?
What is the process of removing fibrin called?
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What are the three indices used to classify anemia?
What are the three indices used to classify anemia?
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Which coagulation pathway is initiated by tissue damage?
Which coagulation pathway is initiated by tissue damage?
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Which coagulation pathway is initiated by exposure of blood to a negatively charged surface?
Which coagulation pathway is initiated by exposure of blood to a negatively charged surface?
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Which coagulation pathway converges into the formation of factor Xa?
Which coagulation pathway converges into the formation of factor Xa?
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Which coagulation factor is involved in the conversion of fibrinogen to fibrin?
Which coagulation factor is involved in the conversion of fibrinogen to fibrin?
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Which coagulation factor is involved in the stabilization of the fibrin clot?
Which coagulation factor is involved in the stabilization of the fibrin clot?
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What is the process of removing fibrin called?
What is the process of removing fibrin called?
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Which pathway involves coagulation factors XI, XII, PK, and HK?
Which pathway involves coagulation factors XI, XII, PK, and HK?
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What is the function of the fibrinogen group of coagulation factors?
What is the function of the fibrinogen group of coagulation factors?
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Which coagulation factors are vitamin K dependent?
Which coagulation factors are vitamin K dependent?
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Where do most coagulation reactions occur?
Where do most coagulation reactions occur?
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What is the classification of erythrocytes based on their size and hemoglobin content called?
What is the classification of erythrocytes based on their size and hemoglobin content called?
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What is the first stage of hemostasis?
What is the first stage of hemostasis?
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Which pathway involves tissue factor and coagulation factors VII, X, and V?
Which pathway involves tissue factor and coagulation factors VII, X, and V?
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What is the function of the contact group of coagulation factors?
What is the function of the contact group of coagulation factors?
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What is the process of transforming soluble fibrinogen into insoluble fibrin called?
What is the process of transforming soluble fibrinogen into insoluble fibrin called?
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Which group of coagulation factors is involved in fibrinolysis?
Which group of coagulation factors is involved in fibrinolysis?
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What are the three indices used to classify anemia?
What are the three indices used to classify anemia?
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What are the two stages of hemostasis?
What are the two stages of hemostasis?
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What is the function of the fibrinogen group of coagulation factors?
What is the function of the fibrinogen group of coagulation factors?
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Which coagulation factors are contained in the Prothrombin group?
Which coagulation factors are contained in the Prothrombin group?
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Where do most coagulation reactions occur?
Where do most coagulation reactions occur?
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What is the function of the contact group of coagulation factors?
What is the function of the contact group of coagulation factors?
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What is fibrinolysis?
What is fibrinolysis?
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What are the three indices used to classify anemia?
What are the three indices used to classify anemia?
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Which coagulation mechanism pathway is activated by tissue damage?
Which coagulation mechanism pathway is activated by tissue damage?
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What are the two pathways involved in the coagulation mechanism?
What are the two pathways involved in the coagulation mechanism?
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What is the function of the platelet plug in hemostasis?
What is the function of the platelet plug in hemostasis?
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What are the three groups of coagulation proteins?
What are the three groups of coagulation proteins?
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What is the function of the intrinsic pathway in the coagulation mechanism?
What is the function of the intrinsic pathway in the coagulation mechanism?
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Is hemostasis a process that involves two stages?
Is hemostasis a process that involves two stages?
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Does primary hemostasis involve the formation of a stable platelet plug?
Does primary hemostasis involve the formation of a stable platelet plug?
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Does secondary hemostasis involve the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
Does secondary hemostasis involve the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin?
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Are coagulation proteins divided into two groups?
Are coagulation proteins divided into two groups?
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Which group of coagulation proteins contains vitamin K dependent factors?
Which group of coagulation proteins contains vitamin K dependent factors?
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Which group of coagulation proteins contains coagulation factors I, V, VIII, and XIII?
Which group of coagulation proteins contains coagulation factors I, V, VIII, and XIII?
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What is the function of the contact group of coagulation factors?
What is the function of the contact group of coagulation factors?
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Do most coagulation reactions occur on the surface membrane of activated platelets?
Do most coagulation reactions occur on the surface membrane of activated platelets?
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Is fibrinolysis the process of removing fibrin that is initiated when clotting begins?
Is fibrinolysis the process of removing fibrin that is initiated when clotting begins?
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Do the erythrocyte indices help classify erythrocytes based on their size and hemoglobin content?
Do the erythrocyte indices help classify erythrocytes based on their size and hemoglobin content?
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How many indices are used to classify anemia?
How many indices are used to classify anemia?
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What are the three indices used to classify anemia?
What are the three indices used to classify anemia?
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Primary hemostasis involves the formation of a stable platelet plug.
Primary hemostasis involves the formation of a stable platelet plug.
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Secondary hemostasis involves the transformation of soluble fibrinogen into insoluble fibrin.
Secondary hemostasis involves the transformation of soluble fibrinogen into insoluble fibrin.
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Coagulation mechanism involves only intrinsic and extrinsic pathways.
Coagulation mechanism involves only intrinsic and extrinsic pathways.
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The prothrombin group contains coagulation factors II, VII, IX, and X.
The prothrombin group contains coagulation factors II, VII, IX, and X.
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The fibrinogen group contains coagulation factors II, V, VIII, and XIII.
The fibrinogen group contains coagulation factors II, V, VIII, and XIII.
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The contact group includes coagulation factors XI, XII, PK, and HK.
The contact group includes coagulation factors XI, XII, PK, and HK.
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All coagulation reactions occur on the surface membrane of activated platelets.
All coagulation reactions occur on the surface membrane of activated platelets.
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Fibrinolysis is the process of removing platelets from the site of injury.
Fibrinolysis is the process of removing platelets from the site of injury.
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Erythrocyte indices help classify erythrocytes based on their shape and size.
Erythrocyte indices help classify erythrocytes based on their shape and size.
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The three indices used to classify anemia are MCV, MCH, and MCHC.
The three indices used to classify anemia are MCV, MCH, and MCHC.
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Primary thrombocytosis is characterized by excessive platelet production.
Primary thrombocytosis is characterized by excessive platelet production.
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Fibrinogen is a vitamin K dependent coagulation factor.
Fibrinogen is a vitamin K dependent coagulation factor.
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What are the two stages of hemostasis and what does each stage involve?
What are the two stages of hemostasis and what does each stage involve?
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What are the three pathways involved in the coagulation mechanism?
What are the three pathways involved in the coagulation mechanism?
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What are the three groups of coagulation proteins and which factors are included in each group?
What are the three groups of coagulation proteins and which factors are included in each group?
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Where do most coagulation reactions occur?
Where do most coagulation reactions occur?
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What is fibrinolysis and when is it initiated?
What is fibrinolysis and when is it initiated?
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What are erythrocyte indices and how do they help classify erythrocytes?
What are erythrocyte indices and how do they help classify erythrocytes?
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What are the three indices used to classify anemia?
What are the three indices used to classify anemia?
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What is the function of the platelet plug in hemostasis?
What is the function of the platelet plug in hemostasis?
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What are the intrinsic and extrinsic pathways in the coagulation mechanism?
What are the intrinsic and extrinsic pathways in the coagulation mechanism?
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What is the role of vitamin K in the coagulation mechanism?
What is the role of vitamin K in the coagulation mechanism?
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What is the role of the contact group in the coagulation mechanism?
What is the role of the contact group in the coagulation mechanism?
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What is the function of fibrin in the coagulation mechanism?
What is the function of fibrin in the coagulation mechanism?
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- Hemostasis involves ______ stages: primary and secondary.
- Hemostasis involves ______ stages: primary and secondary.
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- Primary hemostasis involves the formation of an ______ platelet plug.
- Primary hemostasis involves the formation of an ______ platelet plug.
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- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into ______ fibrin.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into ______ fibrin.
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- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and ______ pathways.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and ______ pathways.
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- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and ______ group.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and ______ group.
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- Prothrombin group contains vitamin K dependent coagulation factors ______, VII, IX, and X.
- Prothrombin group contains vitamin K dependent coagulation factors ______, VII, IX, and X.
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- Fibrinogen group contains coagulation factors I, V, VIII, and ______.
- Fibrinogen group contains coagulation factors I, V, VIII, and ______.
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- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and ______.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and ______.
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- Most coagulation reactions occur on the surface membrane of ______ platelets.
- Most coagulation reactions occur on the surface membrane of ______ platelets.
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- Fibrinolysis is the process of removing ______ and is initiated when clotting begins.
- Fibrinolysis is the process of removing ______ and is initiated when clotting begins.
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- The erythrocyte indices help classify erythrocytes based on their ______ and hemoglobin content.
- The erythrocyte indices help classify erythrocytes based on their ______ and hemoglobin content.
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- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
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What is the major humeral factor regulating megakaryocyte and platelet development?
What is the major humeral factor regulating megakaryocyte and platelet development?
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What is the first stimulation for platelet activation?
What is the first stimulation for platelet activation?
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What are the four zones of platelet ultra-structure?
What are the four zones of platelet ultra-structure?
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What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
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What is the process that requires several activation events, including adhesion, shape change, secretion, and aggregation?
What is the process that requires several activation events, including adhesion, shape change, secretion, and aggregation?
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What is the function of platelets in maintaining blood vessel integrity?
What is the function of platelets in maintaining blood vessel integrity?
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What is the name of the precursor cells in the bone marrow that give rise to platelets?
What is the name of the precursor cells in the bone marrow that give rise to platelets?
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What is the process that involves the interaction between platelets and coagulation proteins to form secondary hemostatic plugs?
What is the process that involves the interaction between platelets and coagulation proteins to form secondary hemostatic plugs?
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What is the name of the cytokines and growth factors that affect megakaryocyte development?
What is the name of the cytokines and growth factors that affect megakaryocyte development?
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What connects two platelets during platelet adhesion?
What connects two platelets during platelet adhesion?
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What is the name of the process that dissolves fibrin clots and restores blood flow?
What is the name of the process that dissolves fibrin clots and restores blood flow?
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What is the name of the platelet activation event that involves changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid?
What is the name of the platelet activation event that involves changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid?
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What is the major humeral factor regulating megakaryocyte and platelet development?
What is the major humeral factor regulating megakaryocyte and platelet development?
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What are platelets?
What are platelets?
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What is the first stimulation for platelet activation?
What is the first stimulation for platelet activation?
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What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
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What is the function of platelets in maintaining blood vessel integrity and healing injured tissue?
What is the function of platelets in maintaining blood vessel integrity and healing injured tissue?
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What are the three phases of hemostasis?
What are the three phases of hemostasis?
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What is the major humeral factor regulating megakaryocyte and platelet development?
What is the major humeral factor regulating megakaryocyte and platelet development?
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What is the role of fibrinogen in platelet adhesion?
What is the role of fibrinogen in platelet adhesion?
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What is platelet aggregation?
What is platelet aggregation?
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What are platelets?
What are platelets?
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What is the role of platelet granule release in activating platelets?
What is the role of platelet granule release in activating platelets?
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What is the first stimulation for platelet activation?
What is the first stimulation for platelet activation?
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What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
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What are the four zones of platelet ultra-structure?
What are the four zones of platelet ultra-structure?
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What is the process of the formation of the platelet plug?
What is the process of the formation of the platelet plug?
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What is the function of platelets in maintaining blood vessel integrity and healing injured tissue?
What is the function of platelets in maintaining blood vessel integrity and healing injured tissue?
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What are the three phases of hemostasis?
What are the three phases of hemostasis?
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What is the function of platelet activation?
What is the function of platelet activation?
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What is the role of fibrinogen in platelet adhesion?
What is the role of fibrinogen in platelet adhesion?
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What is platelet aggregation?
What is platelet aggregation?
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What is the role of platelet granule release in activating platelets?
What is the role of platelet granule release in activating platelets?
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What are the four zones of platelet ultra-structure?
What are the four zones of platelet ultra-structure?
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What is the process of the formation of the platelet plug?
What is the process of the formation of the platelet plug?
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What is the function of platelet activation?
What is the function of platelet activation?
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What is the major humeral factor regulating megakaryocyte and platelet development?
What is the major humeral factor regulating megakaryocyte and platelet development?
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What are platelets and where are they derived from?
What are platelets and where are they derived from?
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What is the platelet ultra-structure divided into?
What is the platelet ultra-structure divided into?
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What is the function of platelets?
What is the function of platelets?
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What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
What is the result of the interaction between the blood vessel, platelets, and coagulation proteins?
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What are the three phases of hemostasis?
What are the three phases of hemostasis?
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What is the first stimulation for platelet activation?
What is the first stimulation for platelet activation?
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What does platelet activation include?
What does platelet activation include?
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What connects two platelets during platelet adhesion?
What connects two platelets during platelet adhesion?
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What facilitates platelet granule release into surrounding tissues, activating platelets?
What facilitates platelet granule release into surrounding tissues, activating platelets?
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What are the activation events required for the formation of the platelet plug?
What are the activation events required for the formation of the platelet plug?
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What are the cytokines and growth factors that affect megakaryocyte development?
What are the cytokines and growth factors that affect megakaryocyte development?
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Platelets are cells that contain a nucleus.
Platelets are cells that contain a nucleus.
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Thrombopoietin is the major factor regulating megakaryocyte and platelet development.
Thrombopoietin is the major factor regulating megakaryocyte and platelet development.
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Platelets are responsible for maintaining blood vessel integrity.
Platelets are responsible for maintaining blood vessel integrity.
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The platelet ultra-structure is divided into three zones.
The platelet ultra-structure is divided into three zones.
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Secondary hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
Secondary hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
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Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
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Platelet activation does not include changes in surface receptor.
Platelet activation does not include changes in surface receptor.
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Platelet aggregation is the joining of red blood cells together.
Platelet aggregation is the joining of red blood cells together.
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Fibrinogen connects two platelets during platelet adhesion.
Fibrinogen connects two platelets during platelet adhesion.
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Platelet granule release is not involved in the formation of the platelet plug.
Platelet granule release is not involved in the formation of the platelet plug.
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The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
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Fibrinolysis is not one of the three phases of hemostasis.
Fibrinolysis is not one of the three phases of hemostasis.
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Platelets are cells derived from precursor cells in the bone marrow called Megakaryocyte.
Platelets are cells derived from precursor cells in the bone marrow called Megakaryocyte.
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Thrombopoietin is the major humeral factor regulating erythrocyte and platelet development.
Thrombopoietin is the major humeral factor regulating erythrocyte and platelet development.
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Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte.
Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte.
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The platelet ultra-structure is divided into three zones: peripheral zone, structural zone, and membrane system.
The platelet ultra-structure is divided into three zones: peripheral zone, structural zone, and membrane system.
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Platelets help maintain blood vessel integrity, but do not aid in healing injured tissue.
Platelets help maintain blood vessel integrity, but do not aid in healing injured tissue.
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Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins, but not fibrinolysis.
Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins, but not fibrinolysis.
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Secondary hemostasis is the phase of hemostasis that involves platelet activation.
Secondary hemostasis is the phase of hemostasis that involves platelet activation.
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Platelet adhesion to sub-endothelium is the last stimulation for platelet activation.
Platelet adhesion to sub-endothelium is the last stimulation for platelet activation.
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Platelet shape changes from disc-shaped to spiny spheres without pseudopods.
Platelet shape changes from disc-shaped to spiny spheres without pseudopods.
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Fibrinogen connects two platelets during platelet aggregation.
Fibrinogen connects two platelets during platelet aggregation.
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Platelet granule release facilitates platelet granule release into surrounding tissues, inhibiting platelet activation.
Platelet granule release facilitates platelet granule release into surrounding tissues, inhibiting platelet activation.
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The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation, but not platelet granule release.
The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation, but not platelet granule release.
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What is the source of platelets and where are they derived from?
What is the source of platelets and where are they derived from?
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What are platelets and what is their structure?
What are platelets and what is their structure?
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What is the major humeral factor regulating megakaryocyte and platelet development?
What is the major humeral factor regulating megakaryocyte and platelet development?
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What is hemostasis and what are the three phases of hemostasis?
What is hemostasis and what are the three phases of hemostasis?
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What is the first stimulation for platelet activation?
What is the first stimulation for platelet activation?
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What changes occur during platelet activation?
What changes occur during platelet activation?
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What is fibrinogen's role in the formation of the platelet plug?
What is fibrinogen's role in the formation of the platelet plug?
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What are the events required for the formation of the platelet plug?
What are the events required for the formation of the platelet plug?
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What are the functions of platelets in maintaining hemostasis?
What are the functions of platelets in maintaining hemostasis?
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What are the cytokines and growth factors that affect megakaryocyte development?
What are the cytokines and growth factors that affect megakaryocyte development?
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What is the role of platelet granule release in activating platelets?
What is the role of platelet granule release in activating platelets?
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What is the ultra-structure of platelets?
What is the ultra-structure of platelets?
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Platelets are membrane-bound anucleate fragments of cytoplasm of ______
Platelets are membrane-bound anucleate fragments of cytoplasm of ______
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The major humeral factor regulating megakaryocyte and platelet development is ______
The major humeral factor regulating megakaryocyte and platelet development is ______
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The platelet ultra-structure divided into four zones: ______, structural zone, organelle zone, and membrane system
The platelet ultra-structure divided into four zones: ______, structural zone, organelle zone, and membrane system
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Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and ______ proteins to form primary and secondary hemostatic plugs
Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and ______ proteins to form primary and secondary hemostatic plugs
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Primary hemostasis, secondary hemostasis, and ______ are the three phases of hemostasis
Primary hemostasis, secondary hemostasis, and ______ are the three phases of hemostasis
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Platelet adhesion to sub-endothelium is the first stimulation for ______ activation
Platelet adhesion to sub-endothelium is the first stimulation for ______ activation
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Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and ______ is the joining of platelets together
Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and ______ is the joining of platelets together
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Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, ______ platelets
Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, ______ platelets
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The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and ______
The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and ______
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Several ______ and growth factors affect megakaryocyte development
Several ______ and growth factors affect megakaryocyte development
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Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane ______
Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane ______
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Platelets are the smallest circulating hematological elements, derived from precursor cells in the ______ called Megakaryocyte
Platelets are the smallest circulating hematological elements, derived from precursor cells in the ______ called Megakaryocyte
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- Platelets are derived from precursor cells in the bone marrow called ______.
- Platelets are derived from precursor cells in the bone marrow called ______.
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- Platelets are ______ fragments of cytoplasm of megakaryocyte, not truly cells.
- Platelets are ______ fragments of cytoplasm of megakaryocyte, not truly cells.
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- The major humeral factor regulating megakaryocyte and platelet development is ______.
- The major humeral factor regulating megakaryocyte and platelet development is ______.
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- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form ______ and secondary hemostatic plugs.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form ______ and secondary hemostatic plugs.
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- Hemostasis is the result of the interaction between the ______, platelets, and coagulation proteins.
- Hemostasis is the result of the interaction between the ______, platelets, and coagulation proteins.
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- Platelet adhesion to sub-endothelium is the first stimulation for ______ activation.
- Platelet adhesion to sub-endothelium is the first stimulation for ______ activation.
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- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and ______ phospholipid.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and ______ phospholipid.
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- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and ______ is the joining of platelets together.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and ______ is the joining of platelets together.
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- Fibrinogen connects two platelets during platelet adhesion, and ______ release facilitates platelet granule release into surrounding tissues, activating platelets.
- Fibrinogen connects two platelets during platelet adhesion, and ______ release facilitates platelet granule release into surrounding tissues, activating platelets.
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- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and ______.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and ______.
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- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and ______ system.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and ______ system.
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- [Blank] is the process of breaking down the fibrin clot formed during hemostasis.
- [Blank] is the process of breaking down the fibrin clot formed during hemostasis.
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What is the origin of platelets and what are they made of?
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What factors affect megakaryocyte development and what is the major humeral factor regulating it?
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How is the platelet ultra-structure divided and what are its components?
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What are the functions of platelets in the body?
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What is hemostasis and what are the three phases of hemostasis?
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What is the first stimulation for platelet activation?
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What changes occur during platelet activation?
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What happens to the shape of platelets during activation and what is aggregation?
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What is the role of fibrinogen during platelet adhesion and what is platelet granule release?
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What events are required for the formation of the platelet plug?
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What are the major factors that regulate megakaryocyte and platelet development?
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What is the structure of platelets and what are the zones of platelet ultra-structure?
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What is the primary function of platelets in hemostasis?
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What are the agonists that platelets have receptors for?
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What is the procoagulant action of platelets?
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What is the final step of coagulation?
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Which pathway of coagulation is activated by exposed collagen?
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What is the role of factor XIII in hemostasis?
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What laboratory test is used to evaluate the extrinsic pathway of coagulation?
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What is the role of tissue factor pathway inhibitor (TFPI) in hemostasis?
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What is the crucial protein in the initiation of blood coagulation?
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What is the difference between the intrinsic and extrinsic pathways of coagulation?
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What is the function of proteins C and S in hemostasis?
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What is the function of activated partial thromboplastin time (APTT) in laboratory studies of hemostasis?
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What is the role of platelets in hemostasis?
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What laboratory tests are used to evaluate hemostasis?
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What inhibitory systems modulate blood coagulation?
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What is the crucial protein in the initiation of blood coagulation?
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What is the activated partial thromboplastin time (APTT) used to evaluate?
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What is the role of platelets in hemostasis?
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What is the procoagulant action of platelets?
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What is coagulation specifically responsible for?
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What is the intrinsic pathway of coagulation activated by?
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What is the extrinsic pathway of coagulation activated by?
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What is the role of factor XIII in hemostasis?
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What laboratory tests are used to assess hemostasis?
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What inhibitory systems modulate blood coagulation?
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What is the crucial protein in the initiation of blood coagulation?
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What is the difference between the intrinsic and extrinsic pathways of coagulation?
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What is the role of platelets in hemostasis?
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What is the intrinsic pathway of coagulation activated by?
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What modulates blood coagulation?
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What is the crucial protein in the initiation of blood coagulation?
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What does coagulation refer specifically to in hemostasis?
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What is the first step in platelet recruitment and activation?
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What is the function of the GPIIb/IIIa complex in platelet activation?
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What do platelets secrete during activation?
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What is the function of hemoglobin?
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What is the predominant type of hemoglobin in adults?
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What is the iron-chelated porphyrin ring in hemoglobin that can carry one molecule of oxygen?
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What is the type of hemoglobin that occurs only in the embryonic stage?
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What is glycosylated hemoglobin (HbA1c) used as an indicator of?
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What is the effect of increased oxygen affinity on hemoglobin?
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What is the hemoglobin concentration in the body a result of?
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What are abnormal hemoglobins?
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What is the primary function of hemoglobin?
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What is the composition of hemoglobin?
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What is the relationship between hemoglobin and erythrocytes?
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What determines the type of hemoglobin?
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What is the function of glycosylated hemoglobin (HbA1c)?
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What is the role of heme in hemoglobin?
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What is the difference between alpha-like and non-alpha-like globin chains?
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What is the relationship between hemoglobin synthesis and erythrocyte development?
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What is the effect of increased oxygen affinity on hemoglobin?
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What is the function of hemoglobin?
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What is the composition of hemoglobin?
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What is the predominant hemoglobin in adults?
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What is the iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron?
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What is glycosylated hemoglobin (HbA1c) used for in diabetic patients?
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What is the type of hemoglobin that is the predominant hemoglobin in the fetus and newborn?
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What is the molecule that hemoglobin can carry from tissues to the lungs?
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What is the hemoglobin concentration in the body dependent on?
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What is the difference between alpha-like and non-alpha-like globin chains in hemoglobin?
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What is the function of hemoglobin?
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What is the composition of hemoglobin?
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What is the predominant hemoglobin in adults?
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What is the iron-containing molecule in heme?
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What is the function of glycosylated hemoglobin (HbA1c)?
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What is the oxygen carrying capacity of hemoglobin?
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What is the type of hemoglobin that is predominant in the fetus and newborn?
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What is the role of alpha-like and non-alpha-like globin chains in hemoglobin?
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What is the molecule that can bind to the central ferrous iron in heme?
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What is the approximate volume of erythrocyte occupied by hemoglobin?
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What are the abnormal hemoglobins mentioned in the text?
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What is the stage of erythrocyte development where most hemoglobin is synthesized?
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What is the function of hemoglobin?
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What is the composition of hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c) used for?
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What is the iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron in heme called?
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What is the type of hemoglobin determined by?
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What is the effect of abnormal hemoglobins on oxygen transport and exchange?
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What is the oxygen carrying capacity of each gram of hemoglobin?
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What is the approximate volume of erythrocyte occupied by hemoglobin?
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What is responsible for the different functional and physical properties of hemoglobin?
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What is the reticulocyte capable of producing in terms of hemoglobin synthesis?
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Is hemoglobin responsible for transporting oxygen and facilitating carbon dioxide transport?
Is hemoglobin responsible for transporting oxygen and facilitating carbon dioxide transport?
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Can each gram of hemoglobin carry up to 1.34 ml of oxygen?
Can each gram of hemoglobin carry up to 1.34 ml of oxygen?
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Does hemoglobin occupy approximately 33% of the volume of the erythrocyte and account for 90% of the cell dry weight?
Does hemoglobin occupy approximately 33% of the volume of the erythrocyte and account for 90% of the cell dry weight?
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Does hemoglobin concentration in the body result from a balance between the production and destruction of erythrocytes?
Does hemoglobin concentration in the body result from a balance between the production and destruction of erythrocytes?
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Is hemoglobin a tetrameric molecule composed of four globular protein subunits?
Is hemoglobin a tetrameric molecule composed of four globular protein subunits?
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Does each hemoglobin contain four heme groups?
Does each hemoglobin contain four heme groups?
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Is the composition of the globin chains responsible for the different functional and physical properties of hemoglobin?
Is the composition of the globin chains responsible for the different functional and physical properties of hemoglobin?
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Is HbA the major hemoglobin in adults?
Is HbA the major hemoglobin in adults?
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Is HbA1c used as an indicator of blood glucose level in diabetic patients?
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Is most hemoglobin synthesized in the polychromatic stage?
Is most hemoglobin synthesized in the polychromatic stage?
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Do abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin?
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Does increased oxygen affinity mean hemoglobin releases its oxygen more readily?
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Each gram of hemoglobin can carry 1.34 ml of oxygen.
Each gram of hemoglobin can carry 1.34 ml of oxygen.
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Hemoglobin accounts for 90% of the cell dry weight.
Hemoglobin accounts for 90% of the cell dry weight.
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Hemoglobin concentration in the body is solely determined by the production of erythrocytes.
Hemoglobin concentration in the body is solely determined by the production of erythrocytes.
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Hemoglobin is a tetrameric molecule composed of four protein subunits.
Hemoglobin is a tetrameric molecule composed of four protein subunits.
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Heme is a form of iron that can carry four molecules of oxygen.
Heme is a form of iron that can carry four molecules of oxygen.
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The type of hemoglobin is determined by the composition of its globin chains.
The type of hemoglobin is determined by the composition of its globin chains.
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Glycosylated hemoglobin (HbA1c) is only produced in diabetic patients.
Glycosylated hemoglobin (HbA1c) is only produced in diabetic patients.
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Most hemoglobin is synthesized in the polychromatic stage.
Most hemoglobin is synthesized in the polychromatic stage.
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Abnormal hemoglobins have no effect on oxygen transport and exchange.
Abnormal hemoglobins have no effect on oxygen transport and exchange.
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The primary function of hemoglobin is to transport and exchange respiratory gases.
The primary function of hemoglobin is to transport and exchange respiratory gases.
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Increased oxygen affinity means hemoglobin releases oxygen more readily.
Increased oxygen affinity means hemoglobin releases oxygen more readily.
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Hemoglobin synthesis begins in the orthochromatic stage.
Hemoglobin synthesis begins in the orthochromatic stage.
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What is the function of hemoglobin?
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What is the structure of hemoglobin?
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What is the composition of globin chains in hemoglobin?
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What is the role of heme in hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
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What is the process of hemoglobin synthesis?
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What are abnormal hemoglobins?
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What is the effect of increased oxygen affinity on hemoglobin?
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What is the effect of decreased oxygen affinity on hemoglobin?
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What is the volume of erythrocyte occupied by hemoglobin?
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What is the function of hemoglobin?
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What is the composition of hemoglobin?
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What is heme?
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What are the two types of globin chains that make up hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
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What is the percentage of the volume of the erythrocyte occupied by hemoglobin?
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What is the percentage of the cell dry weight accounted for by hemoglobin?
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What are abnormal hemoglobins?
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What is the oxygen-carrying capacity of each gram of hemoglobin?
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When does hemoglobin synthesis begin and which stage produces the most hemoglobin?
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What is the function of hemoglobin?
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What is the structure of hemoglobin?
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What is heme?
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What are the types of globin chains?
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What determines the different functional and physical properties of hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
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When does hemoglobin synthesis begin?
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Where is most hemoglobin synthesized?
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What is the reticulocyte capable of producing?
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What are the different types of abnormal hemoglobins?
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What is the function of hemoglobin?
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What is hemoglobin made of?
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What is heme?
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What determines the type of hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What are abnormal hemoglobins and what are their effects?
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What is the oxygen-carrying capacity of each gram of hemoglobin?
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What is the volume occupancy of hemoglobin in erythrocytes?
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What is the function of hemoglobin?
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What is the structure of hemoglobin?
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What is heme?
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What are the two types of globin chains in hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
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When does hemoglobin synthesis begin?
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Where is most hemoglobin synthesized?
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What are abnormal hemoglobins?
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What does increased oxygen affinity mean for hemoglobin?
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What is the function of hemoglobin in the body?
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What is the composition of hemoglobin?
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What is the role of heme in hemoglobin?
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What are the two types of globin chains in hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c) and what is its significance?
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At what stage does hemoglobin synthesis begin and where is most hemoglobin synthesized?
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What is the function of reticulocytes in hemoglobin synthesis?
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What are some examples of abnormal hemoglobins?
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What determines the type of hemoglobin in the body?
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What is the significance of oxygen affinity in hemoglobin?
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What is the function of hemoglobin and what gases does it transport?
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What is the structure of hemoglobin and what is its composition?
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What is the role of heme in hemoglobin and how many oxygen molecules can each hemoglobin carry?
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What are the two types of globin chains in hemoglobin and what are their functional and physical properties?
What are the two types of globin chains in hemoglobin and what are their functional and physical properties?
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What is the predominant hemoglobin in the fetus and newborn and what is the major hemoglobin in adults?
What is the predominant hemoglobin in the fetus and newborn and what is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c) and what is its use in diabetic patients?
What is glycosylated hemoglobin (HbA1c) and what is its use in diabetic patients?
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What is the process of hemoglobin synthesis and in which stages of erythrocyte development does it occur?
What is the process of hemoglobin synthesis and in which stages of erythrocyte development does it occur?
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What are the abnormal hemoglobins and what are their effects on oxygen transport and exchange?
What are the abnormal hemoglobins and what are their effects on oxygen transport and exchange?
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What is oxygen affinity in hemoglobin and how does it affect oxygen binding and release?
What is oxygen affinity in hemoglobin and how does it affect oxygen binding and release?
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What is the balance that determines hemoglobin concentration in the body?
What is the balance that determines hemoglobin concentration in the body?
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What is the volume of the erythrocyte that hemoglobin occupies and what is its dry weight contribution?
What is the volume of the erythrocyte that hemoglobin occupies and what is its dry weight contribution?
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What is the amount of oxygen that each gram of hemoglobin can carry?
What is the amount of oxygen that each gram of hemoglobin can carry?
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What is the function of hemoglobin?
What is the function of hemoglobin?
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What is the structure of hemoglobin?
What is the structure of hemoglobin?
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What is heme?
What is heme?
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What are the two types of globin chains present in hemoglobin?
What are the two types of globin chains present in hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
What is glycosylated hemoglobin (HbA1c)?
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When does hemoglobin synthesis begin?
When does hemoglobin synthesis begin?
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When is most hemoglobin synthesized?
When is most hemoglobin synthesized?
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What is the remaining 35% of hemoglobin synthesized by?
What is the remaining 35% of hemoglobin synthesized by?
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What are some abnormal hemoglobins and their effects on oxygen transport and exchange?
What are some abnormal hemoglobins and their effects on oxygen transport and exchange?
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What happens when hemoglobin has increased oxygen affinity?
What happens when hemoglobin has increased oxygen affinity?
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What is the function of hemoglobin?
What is the function of hemoglobin?
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What is the composition of hemoglobin?
What is the composition of hemoglobin?
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What is the role of heme in hemoglobin?
What is the role of heme in hemoglobin?
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What are the two types of globin chains in hemoglobin?
What are the two types of globin chains in hemoglobin?
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What is the predominant hemoglobin in the fetus and newborn?
What is the predominant hemoglobin in the fetus and newborn?
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What is the major hemoglobin in adults?
What is the major hemoglobin in adults?
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What is glycosylated hemoglobin (HbA1c)?
What is glycosylated hemoglobin (HbA1c)?
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When does hemoglobin synthesis begin?
When does hemoglobin synthesis begin?
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When is most hemoglobin synthesized?
When is most hemoglobin synthesized?
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What is abnormal hemoglobin?
What is abnormal hemoglobin?
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What is the oxygen affinity of hemoglobin?
What is the oxygen affinity of hemoglobin?
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What happens when the oxygen affinity of hemoglobin increases?
What happens when the oxygen affinity of hemoglobin increases?
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Hemoglobin can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry ______ molecules of oxygen.
Hemoglobin can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry ______ molecules of oxygen.
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The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the ______ stage.
The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the ______ stage.
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HbF is the predominant hemoglobin in the ______ and newborn.
HbF is the predominant hemoglobin in the ______ and newborn.
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HbA is the major hemoglobin in ______.
HbA is the major hemoglobin in ______.
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Glycosylated hemoglobin (HbA1c) is used as an indicator of ______ level in diabetic patients.
Glycosylated hemoglobin (HbA1c) is used as an indicator of ______ level in diabetic patients.
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Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______, with different causes and effects on oxygen transport and exchange.
Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______, with different causes and effects on oxygen transport and exchange.
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Hemoglobin synthesis begins as early as the ______ stage.
Hemoglobin synthesis begins as early as the ______ stage.
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The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases ______.
The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases ______.
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Increased oxygen affinity means hemoglobin does not give up its ______.
Increased oxygen affinity means hemoglobin does not give up its ______.
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Decreased oxygen affinity means hemoglobin releases its ______ more readily.
Decreased oxygen affinity means hemoglobin releases its ______ more readily.
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Each gram of hemoglobin can carry 1.34 ml of ______.
Each gram of hemoglobin can carry 1.34 ml of ______.
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Hemoglobin concentration in the body results from a balance between the production and destruction of ______.
Hemoglobin concentration in the body results from a balance between the production and destruction of ______.
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Hemoglobin is responsible for transporting ______ from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs
Hemoglobin is responsible for transporting ______ from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs
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Each gram of hemoglobin can carry 1.34 ______ of oxygen
Each gram of hemoglobin can carry 1.34 ______ of oxygen
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Hemoglobin concentration in the body results from a balance between the ______ and destruction of erythrocytes
Hemoglobin concentration in the body results from a balance between the ______ and destruction of erythrocytes
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Hemoglobin is a ______ molecule, composed of four globular protein subunits, each containing a heme group and a globin chain
Hemoglobin is a ______ molecule, composed of four globular protein subunits, each containing a heme group and a globin chain
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Heme is an iron-chelated ______ ring that can carry one molecule of oxygen bound to the central ferrous iron
Heme is an iron-chelated ______ ring that can carry one molecule of oxygen bound to the central ferrous iron
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The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and ______)
The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and ______)
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The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in ______
The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in ______
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Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of ______ level in diabetic patients
Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of ______ level in diabetic patients
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Hemoglobin synthesis begins as early as the ______ stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%
Hemoglobin synthesis begins as early as the ______ stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%
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Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______, with different causes and effects on oxygen transport and exchange
Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______, with different causes and effects on oxygen transport and exchange
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The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and ______ oxygen
The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and ______ oxygen
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Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more ______
Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more ______
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- Hemoglobin is a specialized protein responsible for transporting ______ from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Hemoglobin is a specialized protein responsible for transporting ______ from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
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- Each gram of hemoglobin can carry ______ ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Each gram of hemoglobin can carry ______ ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
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- Hemoglobin concentration in the body results from a balance between the production and destruction of ______.
- Hemoglobin concentration in the body results from a balance between the production and destruction of ______.
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- Hemoglobin is a ______ molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Hemoglobin is a ______ molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
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- Heme is an ______-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- Heme is an ______-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
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- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the ______ stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the ______ stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
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- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood ______ level in diabetic patients.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood ______ level in diabetic patients.
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- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the ______ stage, and the reticulocyte capable of producing the remaining 35%.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the ______ stage, and the reticulocyte capable of producing the remaining 35%.
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- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______ with different causes and effects on oxygen transport and exchange.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and ______ with different causes and effects on oxygen transport and exchange.
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- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases ______.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases ______.
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- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more ______.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more ______.
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- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and ______-like (epsilon, beta, delta, and gamma).
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and ______-like (epsilon, beta, delta, and gamma).
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Study Notes
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Platelet Disorders and Inherited Coagulation Disorders
- Platelets are produced by fragmentation of megakaryocyte cytoplasm in the bone marrow.
- Primary thrombocytosis is an uncontrolled, malignant proliferation of platelets, not in response to thrombopoietin, and can be caused by essential thrombocythemia, polycythemia vera, and chronic myelocytic leukemia.
- Platelet counts can be >1000 X 10 /L in primary thrombocytosis, and it can be associated with hemorrhagic or thrombotic complications.
- Secondary thrombocytosis is characterized by increased platelet production, usually in response to thrombopoietin, and platelet count is elevated, but usually < 1000 X 10 /L.
- Thrombocytopenia is characterized by a platelet count below 100 x 10 /L and can result in abnormal bleeding associated with thrombocytopenia or abnormal platelet function.
- Common platelet disorders include decreased production due to aplastic anemia or tumors and increased destruction due to immune thrombocytopenia, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, or hypersplenism.
- Hereditary platelet function disorders include deficiency of membrane GPIIb, deficiency of GPIb, and absence of α. granules or dense granules.
- Acquired platelet function disorders include antiplatelet drugs, hyperglobulinemia associated with multiple myeloma, myeloproliferative disorders, and uremia in renal failure.
- Hemophilia A is an X-linked recessive condition resulting from a deficiency of factor VIII, and it predominately affects males with symptoms varying depending on the degree of deficiency.
- Hemophilia A laboratory studies show normal platelet count, normal bleeding time, normal PT, and prolonged PTT, and treatment is factor VIII concentrate.
- Von Willebrand disease is an autosomal dominant bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, and clinical features include spontaneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.
- Acquired coagulopathies include vitamin K deficiency and liver disease, while DIC causes widespread microthrombi with the consumption of platelets and clotting factors, causing hemorrhage, and laboratory studies show decreased platelet count, prolonged PT/PTT, decreased fibrinogen, and elevated fibrin split products (D.dimers).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Hemostasis and Coagulation Mechanism
- Hemostasis involves two stages: primary and secondary.
- Primary hemostasis involves the formation of an unstable platelet plug.
- Secondary hemostasis involves the reinforcement of the platelet plug by transforming soluble fibrinogen into insoluble fibrin.
- Coagulation mechanism involves intrinsic pathways, extrinsic pathways, and common pathways.
- Coagulation proteins are divided into three groups: prothrombin group, fibrinogen group, and contact group.
- Prothrombin group contains vitamin K dependent coagulation factors II, VII, IX, and X.
- Fibrinogen group contains coagulation factors I, V, VIII, and XIII.
- Contact group includes coagulation factors XI, XII, PK, and HK and is involved in the initial activation of the intrinsic pathway and fibrinolysis.
- Most coagulation reactions occur on the surface membrane of activated platelets.
- Fibrinolysis is the process of removing fibrin and is initiated when clotting begins.
- The erythrocyte indices help classify erythrocytes based on their size and hemoglobin content.
- The three indices used to classify anemia are mean cell volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC).
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
Overview of Platelets and Primary Hemostasis
- Platelets are the smallest circulating hematological elements, derived from precursor cells in the bone marrow called Megakaryocyte.
- Platelets are membrane-bound anucleate fragments of cytoplasm of megakaryocyte, not truly cells.
- Several cytokines and growth factors affect megakaryocyte development, and the major humeral factor regulating megakaryocyte and platelet development is thrombopoietin.
- The platelet ultra-structure divided into four zones: peripheral zone, structural zone, organelle zone, and membrane system.
- Platelets maintain blood vessel integrity, aid in healing injured tissue, and interact with other platelets and coagulation proteins to form primary and secondary hemostatic plugs.
- Hemostasis is the result of the interaction between the blood vessel, platelets, and coagulation proteins.
- Primary hemostasis, secondary hemostasis, and fibrinolysis are the three phases of hemostasis.
- Platelet adhesion to sub-endothelium is the first stimulation for platelet activation.
- Platelet activation includes changes in metabolic biochemistry, morphology, surface receptor, and membrane phospholipid.
- Platelet shape changes from disc-shaped to spiny spheres with pseudopods, and aggregation is the joining of platelets together.
- Fibrinogen connects two platelets during platelet adhesion, and platelet granule release facilitates platelet granule release into surrounding tissues, activating platelets.
- The formation of the platelet plug requires several activation events, including adhesion, shape change, secretion, and aggregation.
The Role of Platelets and Coagulation in Hemostasis
- Platelets are recruited to damaged blood vessels to form an occlusive plug.
- Platelets have receptors for agonists like collagen and von Willebrand factor, and contain organelles with proteins like fibrinogen and small molecules like ADP.
- Platelet activation leads to aggregation, adhesion, and promotion of further activation.
- Platelets also have a procoagulant action, accelerating the formation of factor Xa and thrombin.
- Coagulation refers specifically to the conversion of fibrinogen to fibrin, resulting in the formation of a stable hemostatic plug.
- Coagulation involves a complex biochemical cascade of proteolytic enzymes (serine proteases) and cofactors.
- The intrinsic pathway is activated by exposed collagen, while the extrinsic pathway involves tissue factor complexing with factor VII.
- Both pathways terminate in the final common pathway where activated factor X converts prothrombin into thrombin, which converts fibrinogen to fibrin.
- Factor XIII crosslinks the fibrin polymer to consolidate the thrombus.
- Laboratory tests of hemostasis include the prothrombin time (PT) and activated partial thromboplastin time (APTT).
- Blood coagulation is modulated by inhibitory systems like anti-thrombin, proteins C and S, and tissue factor pathway inhibitor (TFPI).
- Tissue factor is the crucial protein in the initiation of blood coagulation and activates both the extrinsic and intrinsic pathways.
The Role of Platelets and Coagulation in Hemostasis
- Platelets are recruited to damaged blood vessels to form an occlusive plug.
- Platelets have receptors for agonists like collagen and von Willebrand factor, and contain organelles with proteins like fibrinogen and small molecules like ADP.
- Platelet activation leads to aggregation, adhesion, and promotion of further activation.
- Platelets also have a procoagulant action, accelerating the formation of factor Xa and thrombin.
- Coagulation refers specifically to the conversion of fibrinogen to fibrin, resulting in the formation of a stable hemostatic plug.
- Coagulation involves a complex biochemical cascade of proteolytic enzymes (serine proteases) and cofactors.
- The intrinsic pathway is activated by exposed collagen, while the extrinsic pathway involves tissue factor complexing with factor VII.
- Both pathways terminate in the final common pathway where activated factor X converts prothrombin into thrombin, which converts fibrinogen to fibrin.
- Factor XIII crosslinks the fibrin polymer to consolidate the thrombus.
- Laboratory tests of hemostasis include the prothrombin time (PT) and activated partial thromboplastin time (APTT).
- Blood coagulation is modulated by inhibitory systems like anti-thrombin, proteins C and S, and tissue factor pathway inhibitor (TFPI).
- Tissue factor is the crucial protein in the initiation of blood coagulation and activates both the extrinsic and intrinsic pathways.
Hemoglobin: Structure, Types, Synthesis, and Function
- Hemoglobin is a specialized protein responsible for transporting oxygen from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Each gram of hemoglobin can carry 1.34 ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Hemoglobin concentration in the body results from a balance between the production and destruction of erythrocytes.
- Hemoglobin is a tetrameric molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Heme is an iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and gamma).
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood glucose level in diabetic patients.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin, with different causes and effects on oxygen transport and exchange.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases oxygen.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more readily.
Hemoglobin: Structure, Types, Synthesis, and Function
- Hemoglobin is a specialized protein responsible for transporting oxygen from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Each gram of hemoglobin can carry 1.34 ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Hemoglobin concentration in the body results from a balance between the production and destruction of erythrocytes.
- Hemoglobin is a tetrameric molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Heme is an iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and gamma).
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood glucose level in diabetic patients.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin, with different causes and effects on oxygen transport and exchange.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases oxygen.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more readily.
Hemoglobin: Structure, Types, Synthesis, and Function
- Hemoglobin is a specialized protein responsible for transporting oxygen from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Each gram of hemoglobin can carry 1.34 ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Hemoglobin concentration in the body results from a balance between the production and destruction of erythrocytes.
- Hemoglobin is a tetrameric molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Heme is an iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and gamma).
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood glucose level in diabetic patients.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin, with different causes and effects on oxygen transport and exchange.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases oxygen.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more readily.
Hemoglobin: Structure, Types, Synthesis, and Function
- Hemoglobin is a specialized protein responsible for transporting oxygen from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Each gram of hemoglobin can carry 1.34 ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Hemoglobin concentration in the body results from a balance between the production and destruction of erythrocytes.
- Hemoglobin is a tetrameric molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Heme is an iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and gamma).
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood glucose level in diabetic patients.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin, with different causes and effects on oxygen transport and exchange.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases oxygen.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more readily.
Hemoglobin: Structure, Types, Synthesis, and Function
- Hemoglobin is a specialized protein responsible for transporting oxygen from the lungs to tissues and facilitating carbon dioxide transport from tissues to the lungs.
- Each gram of hemoglobin can carry 1.34 ml of oxygen, and it occupies approximately 33% of the volume of the erythrocyte and accounts for 90% of the cell dry weight.
- Hemoglobin concentration in the body results from a balance between the production and destruction of erythrocytes.
- Hemoglobin is a tetrameric molecule, composed of four globular protein subunits, each containing a heme group and a globin chain.
- Heme is an iron-chelated porphyrin ring that can carry one molecule of oxygen bound to the central ferrous iron, and each hemoglobin can carry four molecules of oxygen.
- The composition of the globin chains is responsible for the different functional and physical properties of hemoglobin, with two types of globin chains: alpha-like (alpha, zeta) and non-alpha-like (epsilon, beta, delta, and gamma).
- The type of hemoglobin is determined by the composition of its globin chains, with some hemoglobins occurring only in the embryonic stage, HbF being the predominant hemoglobin in the fetus and newborn, and HbA being the major hemoglobin in adults.
- Glycosylated hemoglobin (HbA1c) is produced throughout the erythrocyte life cycle and used as an indicator of blood glucose level in diabetic patients.
- Hemoglobin synthesis begins as early as the pronormoblast stage, with most hemoglobin synthesized in the polychromatic stage, and the reticulocyte capable of producing the remaining 35%.
- Abnormal hemoglobins include carboxyhemoglobin, methemoglobin, and sulfhemoglobin, with different causes and effects on oxygen transport and exchange.
- The function of hemoglobin is to transport and exchange respiratory gases, with oxygen affinity determining the ease with which hemoglobin binds and releases oxygen.
- Increased oxygen affinity means hemoglobin does not give up its oxygen, while decreased oxygen affinity means hemoglobin releases its oxygen more readily.
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Test your knowledge on platelet disorders and inherited coagulation disorders with this informative quiz. From primary and secondary thrombocytosis to hereditary and acquired platelet function disorders, this quiz covers a range of important topics. You'll also learn about Hemophilia A, Von Willebrand disease, and acquired coagulopathies like vitamin K deficiency and liver disease. So, if you're interested in understanding more about the causes, symptoms, and treatment of these disorders, take this quiz