Section 5 Flashcards
List the best anticoagulant to use for coagulation specimens. Discuss why this tube must be full.
- Sodium Citrate (binds Ca++)
- This tube must be full to meet critical ratio value (9: 1 anticoagulant )
- (NOT EDTA - degrades Factor)
- Not heparin - inhibits coagulation factors
Discuss how an increased or decreased hematocrit can affect a coagulation specimen
- abnormal Hematocrit will affect the ratio of the blood to anticoagulant and this needs to be adjusted.
- Low Hct - more plasma, need more anticoagulant
- High Hct - less plasma, nee less anticoagulant
Discuss the use of platelet poor plasma (PPP) and platelet rich plasma (PRP) in coagulation studies.
Coagulation studies use platelet poor plasma (PPP):
–> The use of platelet poor plasma helps with clot-based plasma coagulation tests. Platelets greater than 10K will affect clot-based test, for it may trigger the coagulation cascade.
- Platelet studies use platelet rich plasma. PRP is used for light transmittance platelet aggregometry.
List factors by number and common name if preferentially used.
- Factor I, also known as Fibrinogen
- Factor II, Prothrombin
- Factor III, Tissue Factor III (TF III)
- Factor IV, Calcium (Ca++)
- Factor V, Labile Factor
- Factor VII, Proconvertin or Stable factor
- Factor VIII, von Willebrand Factor Complex
- Factor IX, Christmas Factor
- Factor X, Stuart-Prower
- Factor XI
- Factor XII, Hageman factor
- Factor XIII, Fibrin Stabilizing factor
- Prekallikrein (PK), Fletcher Factor
- Hight Molecular Weight Kininogen (HMWK), Fitzgerald factor
- Bradykinins
- Platelet Factor 3 (PF3)
State the site of formation of the coagulation factors
Most are produced in the liver, except:
- TF III (in all tissues)
- Ca++ (food)
- vWF complex (several tissues, mostly liver)
- Bradykinins & Platelet Factor 3
List the “ Magic 4 “ coagulation factor and state the characteristics they have in common
- Factors II, VII, IX, X
- All produced in the liver, all vitamin K dependent, all depleted by Warfarin therapy.
-vitamin k participates in an oxidation run that adds a second carboxyl group to make a complete factor
- Warfarin (includes Coumadin and Jantoven)
- Arrests vitamin k in its storage form and makes it unavailable to produce complete factors.
Describe the mechanism by which oral anticoagulants inhibit the clotting process
- Oral anticoagulants keep vitamin K in storage from and make it unavailable to produce complete factors.
- no complete factors, thus not able to activate the coagulation cascade.
Diagram and discuss the coagulation cascade. Be sure to include: activations, cofactors, and feedback mechanisms of the intrinsic, extrinsic and common pathways.
- Extrinsic (vascular injury): XII, TF3, Ca++
- Intrinsic (vascular injury): Collagen, XII, XI + HMWK, IX, PF3, Ca++, VIII. As well as XII->Pk, XII-> Kalliken with HMWK -> Bradykinins, XIIa –> Plasminogen-> Plasmin.
- Common pathway: X, PF3, Ca++, V, II, I, Ca++, XIII, and cross linked fibrin polymer.
Feedback mechanism:
-VII can activate factor IX
-IIa can activate XI (alternative pathway), as well as VIII, and XIII
List the functions of thrombin
- One of the Magic Four
- responsible for conversion of fibrinogen to fibrin
- activates Factors V, VIII, XI, XIII, Protein C and Thrombin Activatable Fibrinolytic Inhibitor (TAFI)
Discuss how thrombin converts fibrinogen to fibrin. Include products of this conversion, fibrin polymer and cross linked fibrin.
- thrombin (IIa) acts upon the fibrinogen (I) molecule, it splits a small “tip” from the end of two of the polypeptides chains.
- These tips are known as fibrinopeptides A and B
- The remainder of the molecule is known as a fibrin monomer (Ia) (one molecule of fibrin).
- The fibrin monomers will attach to one another (ends to end and side to side) to form fibrin polymer and eventually a visible, solid fibrin clot.
- Thrombin ( with Ca++) activates Factor XIII, thus stabilizes the clot.
Discuss the two major subunits of the factor VIII complex and the function of each.
- Works in complex with IXa, Ca++, and PF3 to activate factor X
- Calcium is the mediator of platelet activation
- Platelet factor 3 provides binding site for citation k depends factors
Be familiar with the Contract factor and their interaction (including the kinins)
- Factor XI, travels in blood coupled with HMWK
- Factor XII, activates Prekalikren to Kallikrein (Kallikrein activates kind & Fibrinolytic pathways.
- Prekallikrein, activates by XIIa, attaches to HMWK and activates Kallikren (more XII, plasminogen to plasmin, hydrozles bradykinins from HMWK to imitate kinin system.
- High Molecular Weight Kininogen (HMWK), complexes with XI and PK –> cofactor with XIIa to activate XI, acts as a substrate for kallirein in the production of kinins
