1. Coagulation tests CBC- complete blood count
PT/INR- prothrombin time and international normalized ratio
aPTT- activated partial thromboplastin time

2. PT/INR Measures extrinsic & common pathways
Range: <1.5x control = no ↑ bleeding risk
> 2.5x control = risk of spont bleeding
Thromboplastin + (TF + phospholipid) + Ca++ + plasma
Measure clotting time
INR: [(PT patient)/(PT lab mean)]ISI

3. aPTT Measures intrinsic and common pathways
Range: <1.5x control = no ↑ bleeding risk
> 2.5x control = risk of spont bleeding
Phospholipid mixture + surface activating agent (glass) + plasma, then + Ca++
Measure clotting time

4. Mixing studies Determines cause of prolonged PT and aPTT
Factor deficiency vs. presence of an inhibitor
Patient plasma diluted 1:1 with normal plasma
Tests repeated immediately with 1 aliquot & 1 hr after incubation at 37ºC with a 2nd aliquot
If PT or aPTT corrected, then patient has factor deficiency
If PT or aPTT not corrected, then an inhibitor likely present
Antibodies to clotting factors time dependent
Other inhibitors not

5. Platelet disorders
Thrombocytopenia- platelet counts of <50,000 cells/uL
↓ platelet production: destruction of marrow
Thrombotic thrombocytopenia purpura: endothelial cells produce ↑ ULvWF that isn’t processed normally into vWF multimers → platelet aggregation & RBC destruction
Heparin-induced thrombocytopenia: non-immune = transient ↓ in platelet count, and immune = IgG binds to platelet factor 4, triggered by i.v. administration of heparin, can → arterial thrombosis
Idiopathic thrombocytopenic purpura: IgG to platelet glycoprotein receptors → opsonization & phagocytosis of platelets

6. Platelet disorders
Thrombocytosis- platelet counts of 500,000 – 1,000,000 cells/uL
Reactive thrombocytosis: caused by surgery, infection, blood loss, iron deficiency or splenectomy; platelets normalize after cause corrected
Essential thrombocytosis: thrombocythemia resulting from clonal stimulation of megakaryocytes or myeloproliferative disorders (myeloid cancers)

7. Platelet disorders Genetic-
Glanzmann thrombasthenia: auto. recessive, receptor doesn’t bind fibrinogen
Bernard-Soulier syndrome: auto. recessive, mutation in vWF receptor, giant platelets
Pseudo-vWD: increased binding of platelets to vWF, which ↓ vWF in plasma
May-Hegglin: auto. dominant, giant platelets & thrombocytopenia

8. von Willebrand disease (vWD)
vWF secreted by platelets & endothelia
Stored in α-granules in platelets
Mediates platelet adhesion in injury & stabilzes factor VIII in plasma
Synthesized as large monomer that is processed into multimers of different sizes
Defect in vWF → ↑ mucocutaneous bleeding, ↑ bleeding after surgery/trauma
3 types:
1 & 2 are autosomal dominant
3 is autosomal recessive