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WEEK 19:

Haemostasis and Coagulation

QuestionAnswer
types of clotting mechanisms intrinsic and extrinsic
intrinsic clotting mechanism activated by trauma in vessel wall
extrinsic clotting mechanism damaged tissue releases thromboplastin
amplification cascade
platelets ]
adhesion slide 9**
aggregation
lab tests (3)
bleeding time incisions to forearm with venous cuff due to thombrocytopenia
prothrombin time (international normalised ratio INR) time for coagulation following addition of thromboplastin
activated partial thromboplastin time (APTT) examines the intrinsic pathway
clotting and bleeding disorders (3) thrombosis, venous, and AF
thrombosis clot unwanted blot clots
venous cloths form in veins (DVT) due to stasis of blood and can travel to lungs) PE
AF risk fo TIA
activated partial thromboplastin time (APTT) altered by (8) changes in factors XII, XI, IX, VIII, X, V, II or I
prothrombin time (international normalised ratio INR) is prolonged by abnormalities of factors VII, X, V, II, or I, liver disease of warfarin
arterial thrombosis (15)
difference between venous and arterial thrombosis venous is more of a coagulation factor event (DVT) but arterial is more of a platelet event (MIs and TIA)
haemophilia types A and B
haemophilia A
haemophilia B deficiemcy of factor IX treated by prophylactic factor X
haemophilia B treatment
haemophilia B A prohylactic factor IX
haemophilia B treatment
Von Willebrand's disease hereditary lack/ defect in WF leading to increased bruising, nose bleeds, and analogue of vasopression ADh nd wWF) and money) gonna joint me lall
liver disease reduced synthesis of blotting blood lead to increased bleeding positionn if not increased for bronthombin time
thrombocytopoeina reduced platllet umber
thrombocytlopenia symptoms idiopathic, viral, drug induced and toxins and skin on motuh
disseminated intravascular coagulation large amount of firbin in pocoagulant material eg aminiotic fluid
factor V kLeiden mutation mararhoron =**
Created by: kablooey
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