Module 2 Exam 1 lecture 5 Flashcards
VTEs are formed where?
In areas of slow distributed flow
T/F stasis blood promotes thrombus
true
what are venous thrombi composed of?
RBC, Fibrin and platelets
how do symptoms of VTE occur?
Flow is obstructed
vascular tissue becomes inflamed
thrombus occurs and affects venous blood flow
Emboli occur and enter pulmonary circulation
Do all DVTs lead to PEs? Do all PEs come from DVTs?
Not all DVTs lead to PEs, but all PEs come from DVTs
What is the virchous triad
3 main things that could cintribute to blood clot development
Name the virchous triad
- Hypercoagulable state- pregnancy, cancer
- Endothelial injury- abnormalities of surface of contact with blood
- Circulatory stasis- abnormalities in blood flow (long periods of immobility)
pathway for the development of VTE
Vessel wall injury (exposure of endothelium)
This triggers platelet adhesion and aggregation
and coagulation cascade is activated
This produces thrombin, triggering fibrin formation
What activates degradation of clot
Tissue plasminogen activator (TPA)
Which factors are procoagulant
VWF, Factor Xa, Factor II (thrombin), factor XIIIa, TF, XIIa
Which factors are anticoag
Heparin, antithrombin, proteins C and S, thrombomodulin
3 phases of coagulation cascade?
Initiation phase
Amplification phase
propagation phase
How is the initiation phase started?
Tissue factor bearing cell is exposed to BV after injury
How is amplification phase started?
BV damage leads to trace amounts of THROMBIN, leading to amplification phase
What is the amplification phase?
Clotting factors become activated developing fibrin clot.