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Can you help me guys. I was reading Kaplan notes and listening to the videos and did not really understand the issue with factor V Leiden.
Also, I've seen a question in Wikitestprep relating Factor V Leiden to Protein C or S!
If you have some info please share :)
 

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1. Factor V is a coagulation factor that stimulate Prothrombin to convert to thrombin .. then activated thrombin causes more fibrin ... this fibrin is a fibrous protein involved in clotting of blood ... so causes hyper-coagulability like thrombosis , DVT , pulmonary embolism ....
2. Protein C is an is a Vit K dependent anticoagulant that inhibits the action of factor V with help of protein S .... thus protein C inhibits the hyper-coagulable state of factor V .....
3. Factor V Leiden is a variant of factor V where factor V is modified .. so protein C cannot inhibit modified factor V ... causes hyper-coagulable states .....
4. When there is protein C deficiency in some patients it cannot inhibit factor V ... causes hypercoagulable states ....
5. In Warfarin therapy it inhibits Vit k dependent factor 2 , 7, 9 , 10 , pr C , pr S .... Usually protein C level drops very fast than other coagulant factor ... as a result decrease natural anti coagulant protein C thus decrease inhibition on factor V causes hypercoagulable states ... which result in skin vascular thrombosis and causes skin necrosis .....
6. If there is factor V deficiency , there will be increase bleeding as ... no factor V to help factor XII to activate prothrombin ... thus decrease coagulation and leads bleeding ....
 

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1. Factor V is a coagulation factor that stimulate Prothrombin to convert to thrombin .. then activated thrombin causes more fibrin ... this fibrin is a fibrous protein involved in clotting of blood ... so causes hyper-coagulability like thrombosis , DVT , pulmonary embolism ....
2. Protein C is an is a Vit K dependent anticoagulant that inhibits the action of factor V with help of protein S .... thus protein C inhibits the hyper-coagulable state of factor V .....
3. Factor V Leiden is a variant of factor V where factor V is modified .. so protein C cannot inhibit modified factor V ... causes hyper-coagulable states .....
4. When there is protein C deficiency in some patients it cannot inhibit factor V ... causes hypercoagulable states ....
5. In Warfarin therapy it inhibits Vit k dependent factor 2 , 7, 9 , 10 , pr C , pr S .... Usually protein C level drops very fast than other coagulant factor ... as a result decrease natural anti coagulant protein C thus decrease inhibition on factor V causes hypercoagulable states ... which result in skin vascular thrombosis and causes skin necrosis .....
6. If there is factor V deficiency , there will be increase bleeding as ... no factor V to help factor XII to activate prothrombin ... thus decrease coagulation and leads bleeding ....
this is the best explanation I heard so far for this mutation. Very nice !!
 
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