Other Flashcards
(34 cards)
Specimen integrity in Bluetop tube
Under filling the tube, high hematocrit, hemolyzed sample
Sodium citrate mechanism of action
Citrate chelates calcium, but much more mildly than EDTA
Alpha-2 macroglobulin
Blocks the activity of factors 2 and 10, causing thrombophilia
Activated protein C resistance
Caused by a point mutation in the F5 gene, factor 5 Leiden, protein C cannot inactivate F5, so clotting continues
Glanzmann’s Thrombasthemia
A hemorrhagic disorder, platelets lack the glycoprotein 2b/3a receptor that binds fibrinogen, causing poor aggregation response with anything but Ristocetin
Also do not show clot retraction
Gray platelet syndrome
Large platelets that lack Alpha granules, causing abnormal aggregation and prolonged bleeding time
Bernard Soulier syndrome
Giant platelets without glycoprotein 1B receptor, does not find VWF well and so does not a tear to side of damage. Does not aggregate with any agonists.
Afibrinogenemia
Inherited fibrinogen deficiency, fibrinogen bridges do not form so platelets do not aggregate
von Willenbrand Disease characteristics
Hereditary bleeding disorder, affecting primary and secondary hemostasis. Needed for platelet adhesion and as a carrier for F8:C. Variable PTT/F8, low VWF antigen, low VWF ristocetin cofactor I say, abnormal platelet aggregation with ristocetin
Platelet aggregation using ristocetin uses the patients platelets, and these have a high affinity for low-dose ristocetin
Tissue factor function
Released from injured endothelial cells and activates F7 to start the extrinsic pathway
Membrane phospholipids in the coagulation process
Phospholipids are contained on the platelet membrane, and provide a surface for contact factor activation
Activate the intrinsic pathway factors 11, 5, and 8 along with calcium
Thrombin action
Thrombin cleaves fibrinogen into a fibrin monomer and fibrinopeptides A and B, the monomers polymerize into a stable fibrin clot
What are the contact factors?
Need a negatively charged service to activate, a complex of factor 12, HMWK, and prekallikrein to activate factor 11
Contact factor deficiencies cause PTT prolongation
Causes of delayed bleeding
Factor 14, antiplasmin deficiency, PAI-1 deficiency
Causes of increased fibrinolysis
Factor 13 deficiency, PAI – 1 deficiency, antiplasmin deficiency, hypofibrinogenemia
Causes of decreased fibrinolysis
TPA deficiency, plasminogen deficiency, increased fibrinogen
Fibrin degradation products
D-dimers and D to D connections only
Fibrinogen/fibrin degradation products
From primary fibrinogenolysis, test for all degradation products
What kind of bleeding problems occur in patients with primary hemostasis defects?
Superficial bleeding in mucous membranes such as guns, nasal cavity, and G.I. tract. They may also exhibit petichiae and bruising.
What kind of bleeding in patients with defects in the secondary hemostasis have?
May have deep bleeding in muscles and joints
What does fibrinogen doing in primary platelet aggregation?
Helps stick together and aggregate in the presence of calcium, this process is reversible until the secondary platelet aggregation occurs
What is platelets released during the secondary platelet aggregation?
Nonmetabolic ADP, is irreversible. Thromboxane A2 and thrombin action activate the release of ADP
What protein is responsible for clot retraction?
Actomyosin = thrombasthenin
How many platelets do megakaryocytes produce?
2000 - 4000
