Hemostasis

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6 HAP II (Cardiovascular Physiology) Flashcards on Hemostasis, created by Jonathan Cash on 05/11/2016.
Jonathan Cash
Flashcards by Jonathan Cash, updated more than 1 year ago
Jonathan Cash
Created by Jonathan Cash about 8 years ago
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Haemostasis Five stages Five phases although some only count the first 3 1. Vascular spasm 2. Platelet plug formation 3. Coagulation or blood clotting. 4. Clot retraction & repair 5. Fibrinolysis
Haemostasis What is it - Blood is normally kept from clotting by flowing smoothly and by chemicals released from endothelial cells. - Haemostasis occurs if a blood vessel breaks or cells in tissue are damaged or blood moves too slowly.
1. Vascular spasm Vasoconstriction triggered by damage to smooth muscle in vessel wall, endothelial cells & platelets. Can last up to 30 minutes
Platelet plug formation - Platelets are Megakaryocyte fragments. - Endothelium normally releases substances to prevent platelets from sticking to each other & vessel wall. - Endothelial damage exposes underlying collagen fibres & Von Willebrand factor sticks them to platelets. - Platelets swell, become sticky & release substances to enhance - > aggregation & spasm -> platelets stickiness & aggregation - The plug alone can stop the bleeding if the wound is small but the plug is loose and not strong
3. Coagulation - Complex positive feedback mechanism - Reinforces the clot to make it strong - Requires13 clotting factors, 12 are plasma proteins made in liver - Factors have both name & roman numeral - Low amounts of any one could result in a blood clotting disorder. Clotting time of 2 -6 mins is normal. - Vitamin K deficiency, poor liver function, inherited trait.
3. Coagulation cont. 2 alternate initiating pathways & then a common pathway Initiating path may be Intrinsic path or extrinsic path Often both are triggered. Both result in activation of factor X (factor ten)
Intrinsic Coagulation - Started within the blood vessel - Initiated by platelets when vessel wall damaged - Contact activation pathway - Slow; 3-6 minutes - 5 steps to activate factor 10
Extrinsic Coagulation - Started outside the blood vessel - Initiated by damaged cells. - Tissue factor pathway - Faster; 15 seconds - 2 steps to activate factor 10
Coagulation Common Pathway Common pathway - Factor X combines with other factors to form thrombin - Thrombin causes Fibrinogen (soluble) to become fibrin (insoluble) - Fibrin strands are cross linked into a fibrin mesh - Fibrin traps & glues RBCs and platelets, reinforcing the clot. - Fibrin causes plasma to become gel - Clot size is limited by thrombin becoming trapped or degraded
4. Clot retraction - 30- 60 minutes after injury - Actin & myosin inside platelets contract pulling fibrin and the wound edges together & squeezing out the serum - Smooth muscle & endothelial cells in blood vessel wall and fibroblasts in surrounding tissue is stimulated to repair damage
5. Fibrinolysis - On skin, the clot becomes a scab and protects the wound underneath. - allows epithelial cells to migrate from the wound edges & colonise the surface under the scab - This thickens and fully regenerates - Picking the scab off removes these new epithelial cells - after 2 days, a fibrin digesting enzyme, begin to dissolve the clot
Tissue Repair - Blood clot is replaced by granulation tissue - made of collagen from fibroblasts - Through which new capillaries grow from the edges - Contractile elements pull wound edges together - If the wound is large, it fills with granulation tissue which becomes a scar. - Bone, epithelial tissue, some connective tissue have an excellent ability to regenerate cells. - Cardiac muscle and nervous tissue have almost no regeneration ability
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