The document discusses evaluation and management of bruising and bleeding conditions. It covers the physiological mechanisms of hemostasis, patterns of bruising and bleeding in different disorders, diagnostic testing including coagulation screening tests, specific bleeding disorders like hemophilia, and treatment of acquired and inherited coagulation factor deficiencies. Case examples are provided to demonstrate evaluation of different clinical bleeding scenarios.
Thrombophilias are hypercoagulable conditions that can be acquired or inherited. Most important hypercoagulable conditions =, testing procedures, duration of anticoagulation will be discussed here. Useful for Internal Medicine Boards and Hematology boards. Some aspects on duration of anticoagulation, HIT are high-yield for USMLE exams.
Thrombophilias are hypercoagulable conditions that can be acquired or inherited. Most important hypercoagulable conditions =, testing procedures, duration of anticoagulation will be discussed here. Useful for Internal Medicine Boards and Hematology boards. Some aspects on duration of anticoagulation, HIT are high-yield for USMLE exams.
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A Survey of IT Usage Patterns in Banks in Jordan 2011 - TABLE OF CONTENTSArab Advisors Group
A ground breaking Arab Advisors’ survey reveals that the Jordanian Banking sector's total cumulative IT budgets totaled US$ 110 million in 2008, 2009 and 2010, averaging 37 million US$ a year.
Surgeons are doing surgeries because of normal blood clotting and wound healing. Suppose if your patient’s blood doesn’t clot properly and you come to know this only on the table, it would be a nightmare to any surgeon irrespective of their subspecialty. In this PPT, I am discussing about how to handle a patient with bleeding diathesis during and after surgery. Indeed it is a challenging and fascinating problem. I hope you will enjoy the video. You can watch all my teaching videos in the following links: surgicaleducator.blogspot.com; youtube.com/c/surgicaleducator.
Surgery in Bleeding disorders- A challenging problem to all surgeonsSelvaraj Balasubramani
Surgery in patients with bleeding disorders like hemophilia is a nightmare to any surgeon. They must have an working knowledge of how to deal these patients in this challenging situation.
Approach to a bleeding disorder: These presentation has the approach for a patient of bleeding disorder. it has History, physical finding, Investigations.
Bleeding disorders Causes, Types, and DiagnosisDr Medical
https://userupload.net/v3l4i8jsk7wq
Factor II, V, VII, X, or XII deficiencies are bleeding disorders related to blood clotting problems or abnormal bleeding problems. Von Willebrand's disease isthe most common inherited bleeding disorder. It develops when the blood lacks von Willebrand factor, which helps the blood to clot.
13. Bleeding Disorder Symptoms Immediate bleeding Delayed bleeding controlled by pressure not controlled by pressure Purpura & petechiae Muscle & joint bleeds Mucosal bleeding Large ecchymoses Epistaxis, menorrhagia Haematuria Bleed after venepuncture Bleed after im injection Post-traumatic bleeds Post-traumatic bleeds GI & CNS bleeds GI & CNS bleeds Platelet / Vascular Defects Clotting Factor Defects
14. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways
15. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways
16. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways – lab assays APTT TCT PT Ca 2+ and phospholipid also required
17. Current & New Anticoagulant Agents Adapted from Weitz JI et al. J Thromb Haemost. 2005;3:1843-1853. Fibrin Fibrinogen Indirect Xa inhibitors Fondaparinux Danaparoid LMWH, UFH Xa Inhibitors : Rivaroxaban Apixaban IIa Inhibitors Ximelagatran Dabigatran ORAL PARENTERAL Xa IIa TF/ VIIa X IX IXa VIIIa Va II Antithrombin Indirect IIa inhibitors UFH, [LMWH] Warfarin FDPs, D-dimer Antithrombin Plasmin
18. Bleeding Disorder Symptoms Immediate bleeding Delayed bleeding controlled by pressure not controlled by pressure Purpura & petechiae Muscle & joint bleeds Mucosal bleeding Large ecchymoses Epistaxis, menorrhagia Haematuria Bleed after venepuncture Bleed after im injection Post-traumatic bleeds Post-traumatic bleeds GI & CNS bleeds GI & CNS bleeds Platelet / Vascular Defects Clotting Factor Defects
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21. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways – Haemophilia APTT TCT PT Isolated deficiency of Factors VIII, IX, XI or XII [intrinsic pathway] causes prolonged APTT with normal PT
29. Disseminated Intravascular Coagulation Systemic activation of coagulation Intravascular deposition of fibrin Depletion of platelets and coagulation factors Thrombosis of small and midsize vessels and organ failure Bleeding
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37. Decline of INR after warfarin cessation when INR >6 Days % INR > 4 Hylek et al. 2000
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41. Case 4 – 64y male 4 days after commencing warfarin for PE
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Editor's Notes
The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
Type of bruise – lumpy or flat, immediate or delayed, bruises, purpura or petechiae Location – soft tissue – subcut or muscle haematoma legs & arms, trunk, back etc
The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.