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Lecture 3

PATH 310 Lecture Notes - Lecture 3: Mutation, Covalent Bond, Hepatocyte


Department
Pathology and Molecular Medicine
Course Code
PATH 310
Professor
Christine Hough
Lecture
3

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Hemophilia: Clinical Aspects
After exposure of tissue factor and initiation of extrinsic pathway, factor 10 is activated
to factor 10a
Prothrobin is actiavted to thrombin
Final reaction in common pathway
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Extrinsic pathway is the initiating one
Positive feedback loop initiated by small amount of thrombin which feeds back and
amplifies the pathway
Factor 8 and 9 occur within this intrinsic feedback loop
The feedback loop is important in developing a normal blood clot
It is switched off by the presence of tissue factor pahway inhibitor
Once the system has been started, it is regulated by this negative inhibitor
Defective Hemostasis in Hemophilia
The extrinsic pathway has been switched off, and the intrinsic pathway is not working
because they are missing either factor 8 or 9
Factor 8 and 9 are essential to produce a normal blood clot
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Procoagulant Complex Formation
Factor 8 and 9 work in this model
Blood coagulation does not occur in the fluid phase, it is limited to surfaces on cells like
blood platelets, endothelial cell injury, blood vessel injury
Cascade of this model
Intrinsic tenase complex
The enzyme is the active form of factor 9
The cofactor is activated factor 8
The substrate is inactive factor 10
This is what is effected in hemophilia
Range of Factor VIII Levels in Plasma
100% is the mean level in more than 20 samples of blood
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