vascular constriction, formation of platelet plug, blood coagulation, clot retraction, clot dissolution
What are the stages of hemostasis?
endothelin-1; vasoconstriction
What substance is released by damaged endothelial cells to initiate ___________.
vascular constriction
-this step's main goal is to stop blood loss
serotonin
Neural spasms are initiated by ________
a
Platelets release _________ upon injury.
a. A2(TXA2)
b. fibrin
c. prothrombin
d. epinephrine
formation of platelet plug
-this step's main goal is to plug blood vessel and start repair process.
blood coagulation
-this step's main goal is to stabilize newly formed plug and form a clot.
glycoproteins GPIIb/IIIa
_________ binds fibrinogen to connect platelets.
a-platelet granules
-contain adhesive factors and growth factors for vessel repair
delta-granules (δ)
- contain vasoconstrictors (histamine, serotonin, epinephrine)
fibrinogen; fibrin
Clotting cascade converts __________ to ________
vitamin k and calcium
Which two molecules are required to synthesize and activate the clotting cascade?
Warfarin
________- reduces vitamin K dependent coagulation factors.
Chelators (citrate and EDTA)
These medications will bind calcium to prevent clot formation.
Heparin
_________ binds to antithrombin III to increase ability to inactivate thrombin and factor Xa
clot retraction
-goal is to shrink clot to join edges of broken vessel
-occurs 20-60 min after clot formation
-platelets contain mitochondria and actin-myosin
-acts similarly to muscle contraction
pulls fibrin strands together and squeezes serum from the clot
Actin-Myosin complex does what to the clot?
clot dissolution
-goal to activate fibrinolysis enzymes to dissolve clot
-plasmin is released from plasminogen and dissolves clot
-ase
Our thrombolytic(anti-clotting) drugs have what common suffix ?
hypercoagulability
-exaggerated form of hemostasis
-predisposes to thrombosis and vessel occlusion
thrombocytosis
-increased platelet function
arterial thrombus
-high shear flow and turbulent blood cause platelet aggregation due to narrowed artery
venous thrombus
-low shear flow and stasis of blood flow cause platelet aggregation and fibrin complexes to activate coagulation cascade
decrease platelet activation; clopidogrel, aspirin, heparin
Treatment for thrombocytosis?
Primary thrombocytosis
-characterized by an excess of unbound thrombopoietin
-stimulates megakaryocyte proliferation
secondary thrombocytosis
-caused by tissue damage due to surgery
-chronic inflammation
-cancer and myeloproliferative disorders (leukemia)
thrombosis, erythromelalgia
clinical manifestations of thrombocytosis?
thrombocytopenia
-decreased platelet number (less than 150,000 thrombocytes)
-increased sequestration of platelets in spleen (more in spleen)
-decrease platelet survival
thrombocytopathia
-impaired platelet function than can have genetic causes (von willebrand disease, hemophilia A, hemophilia B)
-can have acquired disorders that cause it (liver disease)
DIC
-can be caused by paradox disease: clot formations followed by bleeding disorders
-unregulated thrombin generation
-vessel occlusion and tissue ischemia
-widespread hemorrhage
Conditions associated with DIC
-obstetric conditions, cancers, infections, septic shock, trauma or surgery