Lab 1: Coagulation Flashcards
What does a Mixing Study Reveal?
Mixing studies involve combining equal portions of patient plasma and normal pooled plasma
together and repeating the clotting time that was initially prolonged. If the clotting time corrects
when normal pooled plasma is added, it suggests that a factor (or factors) was/were deficient
and have been replaced by the normal plasma. If the clotting time doesn’t correct with a mixing
study, it suggests that there is an inhibitor (typically an antibody or a drug) that is interfering with
the coagulation cascade
IF both the PT and the APTT were prolonged, you would consider deficiencies of:
Common pathway factors (I, II, V, and X)
What are other names for factor I, factor II, factor III?
I - fibrinogen
II - prothrombin
III - thromboplastin (Tissue factor)
Vitamin K-dependent factors are:
II, VII, IX, X, and protein C/S
What drugs cause an aPTT prolongation
Unfractioned heparin, direct Xa inhibitors, direct thrombin inhibitors
Direct Xa inhibitors
rivaroxaban, apixaban, and edoxaban
Direct thrombin inhibitor
parenteral (intravenous) - argatroban and bivalirudin
oral - dabigatran that directly inhibit factor IIa
A 51-year-old patient has a PT of 13.7 s (reference interval = 11-15 s) and an aPTT of 116 s
(reference interval = 25-40 s) with an aPTT 1:1 mixing study result of 38 s (reference interval =
25-40 s).
Based on your knowledge of the coagulation cascade, what could be causing this set of results?
A deficiency of intrinsic pathway factors (factors VIII, IX, XI, and XII)
What drugs cause a PT prolongation
Warfarin, direct Xa inhibitors, and direct thrombin inhibitors
A 25-year-old female has a history of epistaxis and menorrhagia. She also has increased
bleeding from her gums with dental procedures. Her PT is 13.2 s (reference interval = 11-15 s)
and aPTT is 33 s (reference interval = 25-40 s).
von Willebrand Disease (vWD) [primary hemostasis
(typically involving VWF or platelets)] clearly shown with mucocutaneous
bleeding
What is the job of von Willebrand factor in hemostasis
Von Willebrand factor (vWF) binds to and stabilizes factor VIII, increasing the half-life of factor VIII in the circulation. Von Willebrand factor also binds to the subendothelial matrix (particularly collagen) at sites of endothelial damage and promotes platelet adhesion. You can think of vWF as the peanut butter middle of a subendothelial matrix—vWF—platelet sandwich.
Briefly explain the three different types of von Willebrand disease (vWD)
Type 1 and type 3 vWD are quantitative defects in vWF—meaning the affected person doesn’t
make enough vWF.
Type 2 vWD is a heterogenous group of qualitative defects in vWF. Different aspects of vWF
function may be affected, including its ability to bind to platelets, to bind to factor VIII, or to form
the configurations of the vWF molecule that are most effective for hemostasis
ID
He has a prolonged aPTT and corrected mixing study due to a deficiency in an intrinsic pathway factor. Since he has a bleeding phenotype, the most likely factor deficiencies would be factor VIII, IX, or XI. Hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency) are the most common factors.
If our patient is male and has an elevated aPTT time that is corrected in a mixing study. Does that make any difference in how likely you consider some of the
items on your differential diagnosis? (Hint: Are there any that can occur only in males?)
Hemophilia A and B are inherited as X-linked recessive traits and are more likely to affect male
patients or Turner Syndrome where only one X chromosome is present
What factors are Hemophilia A,B, and C respectively
VIII, IX, and XI
