Ha - VTE Flashcards
2 functions of the endothelium
- physical barrier between blood and sub endothelium
- Synthesis of PGI2, TxA2, vWF, tPA
Life span of a platelet? where do they arise?
10 days
Originate in bone marrow. 1 megakaryocyte produces 4000 platelets
Platelet adhesion
a) Directly to sub endothelium via G1pIa
b) via vWF
Platelet aggregation
Platelets are linked via G1pIIb/IIIa
Fibrinogen
Ca2+
Arachidonic acid metabolism - where? What is the product?
Vascular endothelium
PGI2 + TXA2
4 roles of thrombin
- Fibrinogen -> fibrin
- Activates platelets
- Activates factors 5 + 8
- Activates factors 7 + 11 + 13
wtf is the propagation phase
The factor8/9a complex on activated platelets activate factor 10 –> thrombin burst –> fibrinogen converted to fibrin
What is the amplification phase?
The Factor 10/5a complex generates a small amount of thrombin. Thrombin then activates platelets and factors 5, 8, 11, 13
Fibrinolysis pathway?
Plasminogen is converted to plasmin via tPA and urokinase
Plasmin then breaks fibrin into its degradation products
How do antithrombins work? Most active one? which drug is relevant?
Antithrombin binds to and inactivates thrombin to be excreted in the kidney
- Antithrombin III
- Heparin = increases AT function
What is the protein C+S pathway?
Activated protein C complex will inactivate factors 5 + 8
When is the protein C/S pathway defective?
Factor V leiden - Protein C cannot bind to and inactivate it. Therefore hyper coagulable state
TFPI - what does it stand for? what does it do?
Tissue factor pathway inhibitor
binds to and neutralises TF and factor 7a
What is thrombophlebetic syndrome?
recurrent pain, swelling, ulcers
outcomes of a VTE?
5% fatal
20% recur
23% thrombophlebetic syndrome
4% pulmonary HTN
What is virchows triad?
Blood - high viscosity
Vessel wall damage
Static blood flow
causes of thrombophilia
lack of antithrombin / protein C or S
OR
xs coagulation factors / platelets
COMBINED WITH
stimulating factor eg OCP/preg
is the vessel wall pro or antithrombotic? how?
anti - secretes antiplatelets and has no TF expressed
what makes the BV wall thrombotic?
inflammation eg infection/preg/trauma/vasculitis
why does stasis increase VTE?
accumulation of activated factors in the vessel, increased platelet adhesion and leucocytes
also hypoxia induces inflammation
list an immediate and delayed anticoag
immediate = heparin / apixaban
delayed = warfarin
how are DOACs immediate anti coags
anti factor Xa and anti IIa
benefits of DOACs over warfarin
no monitoring needed for DOACs, warfarin needs INR monitoring
how does warfarin act?
Decreases factors 2,7,9,10
which people are at increased risk of thrombosis?
inpatients, cancer / surgical pts, prev VTE, FHx VTE, genetic traits, obsese, elderly
List thromboprophylaxis
LMWH eg enoxaparin
TED stockings
DOACs
How is thrombosis treated
preventing embolus / extension
is INR used to monitor coagulation risk
NO - only for warfarin
