| Question |
Answer |
| half life of thrombocytes |
5 days |
| platelet adhesion binding proteins |
GPIaIIa binds collagen; GPIbIX binds von Willebrand factor; GPIIbIIIa binds fibrinogen to other platelets |
| when are GPIIbIIa receptors exposed on platelets |
during activation |
| action of serotonin |
vasoconstriction |
| action of ADP |
activates other platelets |
| pathway of which COX 1 is part |
phospholipid (phospholipase A2) arachodonic acid (COX1) prostoglandin H2 (thromboxane synthase) thromboxane A2 which activates other platelets |
| pathway of which COX 2 is part |
arachidonic acid (COX2) prostaglandin G2 (protocyclin synthase [PGI]) prostocyclin I2 [PGI2] which leads to inflammation and oppose platelet activation |
| blood clotting factors I, II, III, IV, and XIII |
fibrinogen, prothrombin, tissue factor, calcium, and transglutaminase |
| where are blood clotting factors which are proteases and protease cofactors produced |
liver |
| hemophilia A lacks what |
clotting factor VIII |
| hemophilia B lacks what |
clotting factor IX |
| which clotting cascade and which clotting factors are essential for life |
extrinsic path, tissue factor, and VII/VIIa |
| what activates the intrinsic pathway |
negative surfaces (contact) |
| do you know the clotting cascades? |
if not, go check the notes |
| what does cofactor V do of note |
increase rxn speed of prothrombin to thrombin by 10,000 |
| what does vitamin K do, to what, and where |
add a CO2 to factors II, VII, IX, C, and S; liver |
| what is Calcium's role in clotting |
binds some factors (same that need vit K) to platelets |
| antithrombin |
inhibits thrombin (duh) and factors IXa, Xa, and XIa |
| heparin |
activates antithrombin |
| thrombomodulin location and activity |
surface of intact vascular endothelial cells; binds thrombin and inhibits normal thrombin activity; activates thrombin toward protein C |
| protein C activity |
activated by thrombin and thrombomodulin; inactivates factors V and VIII; protein C is essential |
| plasmin action and plasmin activator |
clot lysis by hydrolyzing fibrin; TPA activates it |
| TPA |
tissue-type plasminogen activator |
| bernard soulier syndrome |
defective vWf receptor (GPIb-IX) |
| Glanzmann's disease |
defective fibrinogen receptor (GPIIb-IIIa) |
| APC stands for what and does what? |
activated protein C; inactivates VIII and V |
| factor V Leiden |
single pt mutation that resists APC inactivation leading to V always being active (thrombosis risk) |
| disfibrinogenemias |
rare cause of bleeding from mutation in fibrinogen |
| acquired bleeding disorders (two types) |
autoantibodies and Vit K dependent |
| anti-coagulants |
calcium chelators (citrate, oxalate) and heparin |
| heparin action and duration |
antithrombin activation, fast acting, lasts for hours |
| vit K antagonists and action |
dicoumarol, warfarin, coumadin (stops vit K from being regenerated which is needed to modify clotting factors) |
| PT is what |
prothrombin time; a clinical lab test to measure extrinsic and common pathways; use INR (international normalized ratio) test/normal: .5 clotting risk, 1 normal, 5 bleeding risk, 10 high bleeding risk |
| PTT or aPTT is what |
(activated) partial thromboplastin time; a measure of the Intrnsic and common pathways; more sensative to heparin than PT; less sensative to vit K than PT |
| natural anticoagulants are produced by |
ticks, hookworms, vampire bats, snakes, leaches |
| coumodin acts like what |
VIKORCI |
| vit K required enzyme |
glutamyl carboxylase |