1. A test for D-Dimer is positive on the serum of a patient.

Why is it true that the

patient has had both thrombotic and fibrinolytic activity occurring somewhere in his
blood vessels? Why is this not necessarily true if only a positive FDP assay is
found?The presence of D-Dimer confirms that fibrinolysis has occurred because they
only occur if fibrin strands from a clot are lysed. Finding FDP only proves that
fibrinogenolysis has occurred. It will be positive even if there was no fibrin clot.

2. What clotting factors must be present to stabilize a fibrin clot that has just formed.
How is this accomplished? Thrombin must activate FXIII and FXIIIa must catalyze the
formation of covalent bonds between fibrin monomers to stabilize the clot.

3. A patient is taking a Vitamin K inhibitor drug (Coumadin) and getting heparin

injections because of deep vein thrombosis. His doctor tells him he is getting
"blood thinners". What's wrong with that statement and what is a better term to use?
Anticoagulant is a better term. The blood does not get thinner from these drugs. There
is instead less chance of a clot forming.

4. You run quantitative immunoassays for FX, FIX, FVII and FII and report values in
the normal range. The patient is taking a Vitamin K inhibitor drug and has an
elevated prothrombin time and INR indicating he might have a bleeding event. Why are
the quantitative assays normal but the PT is not? The proteins (Factors) are still
produced by the hepatocytes and present in normal concentration, but they cannot
undergo the posttranslational change of gamma carboxylation. The extra carboxyl
groups are needed for normal function of the factors. The immunoassays are only
measuring the amount of protein not
functional ability.

5. Plasmin is a very indiscriminant protease, which will actively proteolyse not only
fibrin, but fibrinogen, several other clotting factors, as well as several plasma proteins.
Why does widespread protein destruction not occur when the fibrinolytic system is
activated to dissolve a blood clot? Plasmin is an indiscriminant protease, capable of
degrading a number of plasma proteins. However, in vivo, activation of plasminogen to
plasmin only occurs efficiently in the vicinity of the fibrin clot (to which plasminogen and
plasminogen activators have adsorbed). Any plasmin that diffuses out of the immediate
vicinity of the fibrin clot is quickly complexed with and neutralized by α2-antiplasmin.

6. If vascular injury generates tissue factor, and hemophiliacs (either Factor VIII or Factor IX
deficiency) have an intact "extrinsic pathway," why do hemophiliacs bleed (hemorrhage)
when they cut themselves? Hemophiliacs do have an intact "Extrinsic pathway"
(according to the traditional description of this pathway), and do effectively generate
tissue factor upon vascular injury. The fact that they bleed excessively when their
 vascular system is disrupted (i.e., cut or traumatized) substantiates the importance of
the ability of Factor VIIa to activate Factor IX in hemostasis. The TF/VIIa activation of
Factor X, and subsequent generation of thrombin and fibrin, is insufficient for
hemostasis. Tissue factor activation of coagulation requires both TF/VIIa activation of
Factor X AND Factor IX, in order to achieve and maintain hemostasis in the event of
vessel damage.

7. How does serum differ from plasma? The biggest difference is the consumption of
fibrinogen when plasma clots to form serum. Much of the prothrombin, FV and FVIII is
also consumed in the process.

8. How does serum differ from plasma, i.e., which clotting factors are still present in serum
after plasma clots in a red top tube? The biggest difference is the consumption of
fibrinogen when plasma clots to form serum. Much of the prothrombin, FV and FVIII is
also consumed in the process.