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Overview of haemostasis
/content/chapter/10.22233/9781905319732.chap21
Overview of haemostasis
- Author: Reinhard Mischke
- From: BSAVA Manual of Canine and Feline Haematology and Transfusion Medicine
- Item: Chapter 21, pp 182 - 188
- DOI: 10.22233/9781905319732.21
- Copyright: © 2012 British Small Animal Veterinary Association
- Publication Date: January 2012
Abstract
The haemostatic system is a vital mechanism, the main functions of which are : to guarantee maintenance of vascular integrity, and to maintain blood fluidity under physiological conditions. This chapter considers primary haemostasis; secondary haemostasis (blood coagulation); the cell-based model of blood coagulation; inhibitors of coagulation and fibrinolysis.
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Figures
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21.1
Schematic diagram of haemostasis. (a) Vasoconstriction results in deceleration of blood flow (red blood cells; RBC), which supports adhesion and aggregation of platelets. (b) Further platelets are attracted, leading to complete occlusion by a primary platelet plug. (c) Stabilization by fibrin and cross-linkage of fibrin prevent loss of the clot by increasing blood pressure following decreased vasoconstriction. There is dissolution of boundaries between platelets. (d) Reduction of the size of the clot is caused by retraction of platelets and fibrin strands with near normalization of blood flow. © 2012 British Small Animal Veterinary Association
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21.1
Schematic diagram of haemostasis. (a) Vasoconstriction results in deceleration of blood flow (red blood cells; RBC), which supports adhesion and aggregation of platelets. (b) Further platelets are attracted, leading to complete occlusion by a primary platelet plug. (c) Stabilization by fibrin and cross-linkage of fibrin prevent loss of the clot by increasing blood pressure following decreased vasoconstriction. There is dissolution of boundaries between platelets. (d) Reduction of the size of the clot is caused by retraction of platelets and fibrin strands with near normalization of blood flow.
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21.2
Schematic diagram of the mechanisms underlying platelet adhesion and aggregation. © 2012 British Small Animal Veterinary Association
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21.2
Schematic diagram of the mechanisms underlying platelet adhesion and aggregation.
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21.3
Schematic diagram of the classical cascade model of blood coagulation. HMWK, high molecular weight kininogen; PK, prekallikrein. © 2012 British Small Animal Veterinary Association
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21.3
Schematic diagram of the classical cascade model of blood coagulation. HMWK, high molecular weight kininogen; PK, prekallikrein.
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21.4
The cell-based model of fibrin formation accentuates the role of different cell types in fibrin generation in overlapping phases. (a) The initiation phase on the tissue factor (TF)-bearing cell after exposure of blood to TF-bearing cells at the site of injury results in generation of small amounts of factor (F)IXa and thrombin, which both diffuse away from the TF-bearing cell towards the platelet. (b) Amplification phase. A small amount of thrombin generated on the TF-bearing cell activates platelets, releases von Willebrand factor (vWF) and activates FV, FVIII and FXI. (c) Propagation phase. Activated clotting factors (in phases a and b) assemble on the procoagulant membrane surface of the activated platelet to form intrinsic tenase, which results in FXa generation on the platelet surface. A prothrombinase complex forms and results in the generation of large amounts of thrombin directly on platelets. © 2012 British Small Animal Veterinary Association
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21.4
The cell-based model of fibrin formation accentuates the role of different cell types in fibrin generation in overlapping phases. (a) The initiation phase on the tissue factor (TF)-bearing cell after exposure of blood to TF-bearing cells at the site of injury results in generation of small amounts of factor (F)IXa and thrombin, which both diffuse away from the TF-bearing cell towards the platelet. (b) Amplification phase. A small amount of thrombin generated on the TF-bearing cell activates platelets, releases von Willebrand factor (vWF) and activates FV, FVIII and FXI. (c) Propagation phase. Activated clotting factors (in phases a and b) assemble on the procoagulant membrane surface of the activated platelet to form intrinsic tenase, which results in FXa generation on the platelet surface. A prothrombinase complex forms and results in the generation of large amounts of thrombin directly on platelets.
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21.5
Schematic diagram illustrating the importance of blood flow in the inactivation of thrombin by antithrombin. © 2012 British Small Animal Veterinary Association
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21.5
Schematic diagram illustrating the importance of blood flow in the inactivation of thrombin by antithrombin.
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21.6
The protein C system. APC, activated protein C; PC, protein C; PS, protein S. © 2012 British Small Animal Veterinary Association
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21.6
The protein C system. APC, activated protein C; PC, protein C; PS, protein S.
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21.7
The fibrinolytic system. Activators are indicated in blue boxes; inhibitors of fibrinolysis are indicated in red boxes. © 2012 British Small Animal Veterinary Association
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21.7
The fibrinolytic system. Activators are indicated in blue boxes; inhibitors of fibrinolysis are indicated in red boxes.