4.2 CHESNEY Principles of Coagulation Flashcards Preview

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Flashcards in 4.2 CHESNEY Principles of Coagulation Deck (15):


"reflex" constriction, ATP driven is the vessels first response to injury

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Primary Hemostatsis

-Primary hemostatic plug, with platelet adhesion and fibrinogen, fibrinogen has not yet been polymerized

-Fragile and if not stablized could get washed away by blood eventually

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Secondary Hemostatsis

-See fibrin deposit and stabilization of the clot, driven by tissue factor which activates VII

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Antithrombotic Counter-Regulation

-Here to make sure clotting only takes place where it is needed and keeps clot from becoming to big

-t-Pa (fibrinolysis and thrombomodulin (blocks coag cascade) are released by non-damaged endothelial cells on borders of damage to help keep clot from getting too big



Plasma vs Serum


Plasma: use an anti-coag when it is taken to prevent use of clotting factors

-Serum: has gone through coagulation and does not have any clotting factors left


PT Time

Measure of Extrinsic Pathway: factor VII and common pathway

--VII is a serine protease

-Plasma is taken and rabbit brain thrombopastin and Ca w/ tissue factor are added and machine measures when clott occurs

--Normal time ~12 sec

-If PTT time is normal but the PT time is long then there is a problem with factor VII

-Neither PTT or PT measure factor XIII b/c time stops immediately after a clot is formed

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PTT Time

-Measure of the intrinsic pathway and common pathway, Intrinsic pathway includes XII, XI, IX, VIII

--VIII is a cofactor, XI and IX are serine proteases, V is also a cofactor

-Only XI, IX and VIII deficiencies cause a bleeding disorder, deficiency of XII will not lead to bleeding. XII def will prolong PTT but it will not cause a bleeding disorder

-Factor XIII (transamylase) is not measured, responsible for cross-linking of fibrin to increase tensile strength

-Neither test is very sensitive for fibrinogen, but fibrinogen deficiency will prolong both times, any common pathway deficiency will prolong both times.

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Warfarin and Vitamin K

-factors II (prothrombin) VII, IX, X, protein S and C are all relient on vitamin K for formation

-Warfarin blocks their formation

-Become unalbe to bind Ca and therefore bind membrane


Fragment 1.2

-What is cleaved off of prothrombin during thrombin formation

-Do not know what it does, but has a one to one relationship with thrombin formation, good measure for thrombin formation

-Increased thrombin means a procoag state

-Warfarin will block prothrombin from binding factor V

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vWF def and Hemophilia association with VIII

-Both diseases can be associated with low VIII (hemophilia is the lowest)

-vWF (made by endothelial tiss) is a carrier of VIII, when vWF is absent VIII does not last well alone in circulation, but when vWF is given to patients with def of vWF will see a rise in VIII as it is synthesized by the liver and binds to vWF

-Hemophilia with VIII def will always be low b/c VIII is acutally def

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Actions of Heparin

-heparin can bin antithrombin III (confirmation change) and increase its affinity for thrombin

-antithrombin is an anti-serine protease


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Protein C

-Binds Thrombomodulin Thombin complex along with protein S (cofactor) to platelet surface and inactivates factor V and factor VIII (both are cofactors)

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-Is inhibited by Protein C which leads to more fibrolysis

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-Means that there is cross-linking fibrin formation, they are a product of plasmin breakdown of fibrin

-Fragment D and Y are negative feedback inhibitors and slow down clotting and inhibit platelets

-Presence of D-Dimer means that there has been clot formation

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Endothelial Actions

Just know endothelial can be pro and anti thrombotic

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