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Books on the topic 'Thrombosis; Anticoagulant drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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1

Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York: Oxford University Press, 2006.

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2

Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York, NY: Oxford University Press, 2005.

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3

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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4

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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5

Valentin, Fuster, and Verstraete M, eds. Thrombosis in cardiovascular disorders. Philadelphia: Saunders, 1992.

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6

Thrombosis in cardiovascular diseases. Philadelphia: Saunders, 1992.

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7

Frost & Sullivan., ed. U.S. thrombosis markets: Anticoagulants, antithrombotics, and thrombolytics : new drugs, new indications expand market. Silicon Valley, Mountain View, CA (2525 Charleston Rd., Mountain View, 94043): Frost & Sullivan, 1994.

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8

Wijdicks, Eelco F. M., and Sarah L. Clark. Anticoagulation and Reversal Drugs. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0007.

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Management of anticoagulation, is a common practice. This chapter discusses best approaches, heparin choices, and safety issues. Anticoagulation is required in immobilized patients in the neurosciences intensive care unit to prevent deep venous thrombosis and the more consequential pulmonary embolus. There are very few strong indications for anticoagulation in ischemic stroke and exceptions are discussed. Reversal of anticoagulation is also needed in some patients and certainly in patients with recent significant trauma or spontaneous hemorrhages. Current reversal protocols require intravenous vitamin K, fresh-frozen plasma, and more often, prothrombin complex concentrate. Reversal of the effect of the direct oral anticoagulants is more difficult but options are discussed.
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9

Stanworth, Simon, and Stuart McKechnie. Pathophysiology of disordered coagulation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0269.

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Imbalances in the regulation of haemostasis may manifest as bleeding (depletion of pro-coagulant factors) or thrombosis (deficiency of anti-coagulants). Disordered haemostasis is common in critically-ill patients and may result from infection, trauma, haemorrhage, inflammation, organ dysfunction (notably renal and liver dysfunction), or drug therapy. Complex patterns of coagulopathy where both bleeding and prothrombotic tendencies co-exist are well recognized in critical illness. The limitations of standard laboratory coagulation tests to predict bleeding risk, including activated partial thromboplastin time and prothrombin time, are well recognized. These assays were developed for diagnosis of inherited bleeding disorders or for monitoring of anticoagulant therapy. This has led to increased interest in global haemostatic tests, such as viscoelastic and thrombin generation tests. Thromboembolism is an important cause of morbidity and mortality in critically-ill patients. While inherited causes of bleeding appear to be often related to single gene abnormalities, thrombotic tendencies appear to reflect more complex interactions between inherited and acquired factors. Many interactions exist between coagulation pathways and inflammation. Systemic inflammation triggers widespread activation of coagulation, with pro-inflammatory cytokines activating pro-coagulant pathways and downregulating anticoagulant pathways. A net result of this interaction between inflammatory and coagulation pathways in sepsis is thrombin generation, intravascular fibrin deposition and a consumptive coagulopathy.
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10

Frost & Sullivan., ed. European thrombotic drug markets: Cost containment pressures intensify the competitive environment. Mountain View, Calif: Frost & Sullivan, 1995.

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11

Inpatient Anticoagulation. Wiley-Blackwell, 2011.

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12

1937-, Bell William Robert, Uprichard, Andrew C. G., 1957-, and Gallagher Kim P. 1950-, eds. Antithrombotics. Berlin: Springer, 1998.

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13

Sternbach, Marion. Apheresis in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0268.

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This chapter describes therapeutic plasma exchange, as well as cytapheresis for hyperleukocytosis and essential thrombocythemia, as well as harvesting haematological stem cells (HSC) for transplantation. Instrumentation and techniques are mostly density centrifugation, much less column adsorption for antibodies or membrane filtration for noxious molecules. Pathophysiology of apheresis is dealt with in great detail with emphasis on prevention and treatment of side effects, much more critical in the intensive care unit (ICU) setting. Main manifestations are: hypocalcaemia due to chelation by anticoagulants, hypo- and less hypervolaemia, allergic reactions to sedimenting and volume replacement starches or plasma, depletion of coagulation factors, vitamin K, immunoglobulins, lymphocytes with long lifespan and platelets. Wash-out of drugs for comorbid or underlying conditions occurs inadvertently. Main indications for plasma exchange are thrombotic thrombocytopenic purpura (TTP)/haemolytic uraemic syndrome (HUS) with plasma or cryo-poor supernatant (based on RCT), hyperviscosity syndromes, post-transfusion purpura (PTP) and auto-immune haemolytic anaemia (AIHA), where all other treatments have failed. In cold agglutinin disease, cryoglobulinaemia, coagulation factor inhibitors and ABO incompatible HSC transplants, plasmapheresis has proven useful. Myeloma with renal failure does not seem to benefit significantly from plasma exchange (randomized controlled trials proven).
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14

Fibrinolytic and Antithrombotic Therapy: Theory, Practice, and Management. Oxford University Press, USA, 2000.

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15

Becker, Richard, Green David, and Dan J. Fintel. Antithrombotic Therapy, Third Edition. 3rd ed. Professional Communications, Inc., 2004.

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16

Becker, Richard, Green David, and Dan J. Fintel. Antithrombotic Therapy, Second Edition. 2nd ed. Professional Communications, 2002.

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