disorders of blood coagulation

Question 1

why does our blood clot

Answer 1

prevents pathogens
keep blood in
must be localised fashion 
endothelium has anticoagulant surface 
2 processes of haemostasis = primary or secondary

Question 2

describe primary haemostasis

Answer 2

endothelium releases VWF = circulates in blood and stored in weibel-palade.
if collagen is exposed to blood, VWF binds
platelets have receptors for collagen and VWF, become activated once these bind
activated platelets = functional fibrinogen receptors, needed for aggregation

Question 3

describe secondary haemostasis

Answer 3

activated platelet
tissue factor is expressed by nearly all sub endothelial cells = activates coagulation cascade to initiate minor burst of thrombin
factor FVIIa binds to TF = prothrombin to thrombin
thrombin activates receptors on platelets as well as endothelium, amplifying platelet aggregation
also initiates release of stored VWF from endothelial cells

Question 4

what does increased thrombin production via tenase and prothrombinase contribute to?

Answer 4

contributes fibrinogen to fibrin mesh by thrombin

Question 5

describe fibrinolysis

Answer 5

break down of fibrin
plasminogen activation system

1. plasminogen activated to plasmin by tissue. plasminogen activator = t-PA
2. plasmin degrades fibrin mesh = fibrin degradation products which can be cleared

Question 6

describe natural coagulants

Answer 6

1. antithrombin = serine protease inhibitor. enhanced by binding heparan on endothelial cells

has checkpoints to inhibit coagulation. heparan binding domain = basis of anticoagulant activity of heparan = increases activity of ATIII

2. protein C pathway = protein C and S = natural anticoagulants plasma proteins

protein c is activated by thrombin bound to thrombodulin on endothelial cells to form activated protein c (APC)

protein s = APC cofactor, helps binding to cell surfaces

APC degrades cofactors FVa and FVIIa