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Books on the topic 'Blood coagulation tests'

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Published: 4 June 2021
Last updated: 31 January 2023

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1

Marques, Marisa B. Quick guide to coagulation testing. 2nd ed. Washington, DC: American Association for Clinical Chemistry, 2009.

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2

A, Triplett Douglas, and College of American Pathologists, eds. Advances in coagulation testing: Interpretation and application. Skokie, Ill: College of American Pathologists, 1986.

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3

Jørgen, Jespersen, Bertina Rogier M, and Haverkate F. 1931-, eds. Laboratory techniques in thrombosis: A manual. 2nd ed. Dordrecht: Kluwer Academic Publishers, 1999.

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4

Marques, Marisa B. Quick guide to hemostasis. Washington, DC: American Association for Clinical Chemistry, 2015.

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5

Jørgen, Jespersen, Bertina Rogier M, Haverkate F. 1931-, European Concerted Action on Thrombosis and Disabilities (Committee), and Commission of the European Communities., eds. ECAT assay procedures: A manual of laboratory techniques. Dordrecht: Kluwer Academic Publishers, 1992.

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6

Marques, Marisa B. Quick Guide to Coagulation Testing:. AACC Press, 2006.

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7

Immunoassays in Coagulation Testing. Springer, 2012.

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8

M, Thomson Jean, ed. Blood coagulation and haemostasis: A practical guide. 3rd ed. Edinburgh: Churchill Livingstone, 1985.

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9

M, Thomson Jean, ed. Blood coagulation and haemostasis: A practical guide. 4th ed. Edinburgh: Churchill Livingstone, 1991.

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10

Michael, Laposata, ed. The Clinical hemostasis handbook. Chicago: Year Book Medical Publishers, 1989.

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11

Laboratory Techniques in Thrombosis - A Manual: Second Revised Edition of the Ecat Assay Procedures. 2nd ed. Springer, 1999.

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12

R, Dixon Morris, Brubaker Daniel B, and Blombäck Birger, eds. New advances in hemostasis for transfusion medicine. Arlington, Va: American Association of Blood Banks, 1990.

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13

Kuiper, Gerhardus J. A. J. M., and Hugo ten Cate. Coagulation monitoring. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0266.

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Haemostasis is a dynamic process to stop bleeding after vessel wall damage. Platelets form a platelet plug via activation, adherence, and aggregation processes. The coagulation proteins are activated one-by-one, cascading towards fibrin polymerization, a process controlled by thrombin generation. Fibrinolysis is the process responsible for fibrin mesh degradation, which is also controlled by thrombin. Besides procoagulant proteins, anticoagulant proteins maintain a balance in the haemostatic system. Measuring platelet count and function can be done as part of the monitoring of haemostasis, while coagulation times are measured to assess the coagulation proteins. Degradation products of fibrin and lysis times give information about fibrinolysis. Point-of-care monitoring provides simple, rapid bedside testing for platelets and for whole blood using viscoelasticity properties. In trauma-induced coagulopathy (TIC) platelet counts and coagulation times are still common practice to evaluate haemostasis, but point-of-care measurements are being used more and more. Medication interfering with haemostasis is frequently used in intensive care unit patients. Each (group of) drug(s) has its own monitoring tests either based on classical or novel techniques.
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14

Hendriks, Herman G. D., and Joost T. M. de Wolf. Haematological and coagulation disorders and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0084.

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This chapter covers the principal haematological disorders and their implications for anaesthesia. Haemoglobin concentration is the main determinant of oxygen delivery to the tissues making anaemia a potential concern for the anaesthetist. In deciding whether to correct anaemia with a red blood cell transfusion, the anaesthetist must consider the nature of the surgery and the underling cause of the anaemia as well as the haemoglobin concentration. Techniques to limit the need for blood transfusion and the complications of transfusion are discussed. Perfect haemostasis means control of bleeding without the occurrence of thrombotic events. Coagulation management requires an understanding of this balance and the knowledge that altered coagulation activity may result in clinically relevant bleeding or, in contrast, thrombosis. Therefore, the key in haemostasis is an understanding that every anticoagulant action enhances the risk of bleeding and every procoagulant action enhances the risk of thrombosis. If a specific defect in the haemostatic system is known, treatment is tailored to restore this defect. However, tests to predict surgical bleeding do not exist, as it is for test to predict thrombotic events. The strengths and limitations of coagulation tests should be appreciated before they are used to assist clinical decision-making in the perioperative period. An excellent coagulation test is the clinical field (i.e. the surgical wound). If there are abnormalities in the coagulation tests without clinical bleeding, a correction is hardly necessary. In patients taking anticoagulant medication, consideration must be given on an individual patient basis, to the relative risks of continuing (bleeding) or stopping (thrombotic events) the medication.
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15

Devlin, Hugh, and Rebecca Craven. Blood. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759782.003.0010.

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The blood in relation to dentistry is the topic of this chapter. Components of blood are described, including the blood cell types, their development and functions. Anaemias are discussed and their dental implications. Haemostasis and the coagulation pathway are described, followed by the bleeding disorders, how they are detected in blood tests and managed so as to avoid complications arising from dental treatment. The main malignancies of white blood cells are described in relation to dental care. The final section deals with blood and tissue types and their relevance to blood transfusion and tissue transplantation.
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16

Lewis, S. M., A. M. H. P. van den Besselaar, and H. R. Gralnick. Thromboplastin Calibration and Oral Anticoagulant Control. Springer, 2012.

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17

Lewis, S. M., A. M. H. P. van den Besselaar, and H. R. Gralnick. Thromboplastin Calibration and Oral Anticoagulant Control. Springer Netherlands, 2011.

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18

Assessing Anticoagulant Resistance in Rats and Coagulation Effects in Birds Using Small-Volume Blood Samples. Not Avail, 2005.

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19

Lusher, Jeanne M., and Marion I. Barnhart. Acquired Bleeding Disorders in Children: Platelet Abnormalities and Laboratory Methods. Aperture, 1985.

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20

(Editor), J. Jespersen, R. M. Bertina (Editor), and F. Haverkate (Editor), eds. ECAT Assay Procedures. A Manual of Laboratory Techniques: European Concerted Action on Thrombosis and Disabilities of the Commission of the European Communities. Springer, 1992.

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21

Matthey, Dr Francis. Anticoagulation and transfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00012.

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Chapter 12 covers anticoagulation and transfusion as they present in the acutely unwell patient, and includes information about the coagulation cascade and coagulation tests, hypercoagulable disorders, anticoagulation, factors contributing to coagulation failure and DIC, blood and blood components, bleeding disorders, and transfusion and management of bleeding.
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22

Adam, Sheila, Sue Osborne, and John Welch. Haematological problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0012.

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This chapter discusses specific haematological disorders that require the patient to be admitted to the critical care unit. It describes the normal physiology of blood cells, clotting mechanisms, and fibrinolysis, and the management of related conditions such as thrombocytopenia, leukaemia, and clotting disorders such as disseminated intravascular coagulation. It also includes the management of the critical care patient with haematological malignancy. Specific therapies such as plasma exchange and anticoagulation therapy are discussed in detail and the monitoring of coagulation tests is explained. The chapter also describes the administration of blood and blood products, together with their associated hazards, and the effects of massive transfusions of blood.
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23

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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24

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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25

Medforth, Janet, Linda Ball, Angela Walker, Sue Battersby, and Sarah Stables. Maternal emergencies during pregnancy, labour, and postnatally. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754787.003.0022.

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Maternal emergencies during pregnancy, labour, birth, and the postnatal period are covered. Blood tests during pregnancy and detecting deviations from the norm are included. Maternal emergencies and their management considered include: major obstetric haemorrhage, uterine rupture, eclampsia, emboli (pulmonary embolus and amniotic fluid embolus), HELLP syndrome, disseminated intravascular coagulation, uterine inversion, shock, and maternal resuscitation. Guidelines for admission to a high-dependency unit and current maternal morbidity and mortality data are included.
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26

Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.

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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
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27

Mesquita, Emersom C., and Fernando A. Bozza. Diagnosis and management of viral haemorrhagic fevers in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0293.

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In a globalized scenario where widespread international travel allows viral agents to migrate from endemic to non-endemic areas, health care providers and critical care specialists must be able to readily recognize a suspected case of viral haemorrhagic fever (VHF). Early suspicion is pivotal for improving patient outcome and to ensure that appropriate biosafety measures be applied. VHFs are acute febrile illnesses marked by coagulation disorders and organ specific syndromes. VHFs represent a great medical challenge because diseases are associated with a high mortality rate and many VHFs have the potential for person-to-person transmission (Filoviruses, Arenavioruses, and Bunyaviroses). Dengue is the most frequent haemorrhagic viral disease and re-emergent infection in the world and, due to its public health relevance, severe dengue will receive special attention in this chapter. The diagnosis of VHFs is made by detecting specific antibodies, viral antigens (ELISA) and viral nucleic acid (RT-PCR) on blood samples. Supportive care is the cornerstone in the treatment of VHFs. Ribavirin should be started as soon as a case of VHF is suspected and discontinued if a diagnosis of Filovirus or Flavivirus infection is established. Adjunctive antimicrobial therapy is usually implemented to treat co-existing or secondary infections. Antimalarial treatment should also be initiated if a malaria test (thick blood films) is not quickly available and/or reliable and patients travel history is compatible. It is always recommended to apply appropriate biosafety measures and notify local infection control unit and state and national authorities.
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