Hemostasis Flip Classroom Flashcards
initial investigations for hemostasis concerns
CBC, PBC, PT/INR, PTT, TT, Fibrinogen, LFTs, Creatinine
investigations to assess primary hemostasis
- platelet function tests/ closure times
- platelet aggregation studies
- VWF antigen, VWF activity, FVIII activity
- bleeding time (replaced by CT)
also need to consider bleeding history when deciding how to approach investigation (bleeding or not)
investigations to assess secondary hemostasis
- mixing study
- specific coagulation factor level
- molecular studies.
also need to consider bleeding history when deciding how to approach investigation (bleeding or not)
PTT can be assess the ___ pathway
PT can assess the ____.
a combo assesses the _____
PTT can be assess the INTRINSIC pathway
PT can assess the EXTRINSIC.
a combo assesses the COMMON
*note for card 3. Primary hemostasis refers to platelet aggregation and platelet plug formation. … Secondary hemostasis refers to the deposition of insoluble fibrin, which is generated by the proteolytic coagulation cascade
If prolonged PTT is identified and no bleeding symptoms are present:
If prolonged PTT is identified and there have been bleeding symptoms since childhood:
If prolonged PTT is identified and new onset of bleeding symptoms:
What should you do next?
If prolonged PTT is identified and no bleeding symptoms are present:
- antiphospholipid antibodies, FXII deficincy
If prolonged PTT is identified and there have been bleeding symptoms since childhood:
- congenital factor deficiency
If prolonged PTT is identified and new onset of bleeding symptoms:
- likely acquired factor deficiency
- gotta do a mixing study using pt plasma and normal plasma:
if PTT corrects = factor deficinecy
if PTT remains prolonged = an inhibitor in patient plasma, further testing is needed to determine whether it is an antiphospholipid antibody or an inhibitor to a coagulation factor.
define hemostasis
Hemostasis is an equilibrium between factors that result in either – Blood in a fluid state within the vascular compartment – Formation of blood clots following vascular injury
4 phases of hemostasis
4 phases are regulated in order to achieve hemostatic equilibrium
– Primary hemostasis
– Secondary hemostasis/Coagulation
– Fibrin clot formation and stabilization
– Inhibition of coagulation
what is primary hemostasis
the formation of the platelet plug. 3 steps of platelet plug formation
- adhesion to sub endothelium
- platelet activation
- platelet aggregation.
Describe the steps of platelet plug formation
- adhesion to sub endothelium: Adhesion: Platelets bind to exposed subendothelial VWF through GPIb/IX receptor. During adhesion, VWF in injured endothelium binds to collage to platelet receptor 1b9. VWF has binding sites for platelets and factor 8.
- platelet activation: When platelets are activated, they change shape and release grandule contents that contain hemostatic contents that allows for pro-coagulant form.
- platelet aggregation.Conformational change in platelets can cause aggregation with interactions of fibriogen, forming a platelet plug.
outline secondary hemostasis
involves fibrin clot formation and stabilization. The typical “coagulatioN” pathway
extrinsic pathway: TF is released from injured tissue or endothelial cells or monocytes. When blood comes into contact with TF, Factor 7 binds to TF, Changing to active form.
active factor 7-TF activates clotting factor 9 and 10 (to 9a and 10a). This act produces small amounts of thrombin (2a), which cause a positive cascade within the INTRINSIC system.
Intrinsic pathway: contact factors like TENET (12, 11, 9, 8, 10). Factor 12 also activates factor 11 and then 10 which also helps with production of thrombin.
Amplification:
- thrombin in small quantities in step 1 actives 5, 8, 11. Activates more platelets to ensure adequate surface for coagulation.
Propagation:
- factor 10 is produced when factor 7 activates factor 9. activated Factor 8 and 9 forms the tenase complex to convert factor 10 to its active form.
activated 10 and 5 along with ca2+ and lipid surface from activated platelets form a 5a complex, which produces prothrombin and turns it into thrombin (Factor 2a)
Stabilization:
- the large amounts of thrombin produced converts fibrinogen to soluble fibri which forms soluble clots.
factor 13 is also activated, which links the fibrin molecules together to create an insoluble cross-linked fibrin.
thrombin has the capacity to activate factors:
5, 8, 11.
role of tissue factor pathway inhibitor (TFPI)
inhibits factor 10 and the Tf-Factor 7 complex. Ultimately prevents thrombin activation and subsequent fibrin clot formation
How does protein C and S prevent coagulation
• Activated protein C combins with protein S which inhibited factor 5 and factor 8 (inhibits their active form)
How does antithrombin inhibit the activation of clotting enzymes
• Antithrombin inhibits the activated factor 10 and thrombin, but can also inhibit other factors in the intrinsic factor by forming a complex with the factor. This process is accelerated by the presence of unfracrtionated heparin, which is used to treat excessive clotting.
how does fibrinolysis occur
the fibrinolytic system consisting of PLASMINOGEN and TPA removes the unwanted fibrin clot (turns it into D-Dimers) and restores blood vessel patency once the vascular injury has healed.
