Hemostasis Flashcards
hemostasis
stopping blood loss in response to vascular injury
list the 4 general phases in the process of hemostasis
- vascular constriction
- formation of platelet plug
- formation of blood clot
- fibrous organization
describe and discuss vascular constriction
response to injury to help reduce blood flow/bleeding
describe and discuss formation of the platelet plug
primary hemostasis, platelet adhesion and aggregation, w/ help of vWF and fibrinogen (acts as a bridge for platelets)
describe and discuss formation of the blood clot
secondary hemostasis, activation of clotting factors (clotting cascade), enables fibrin to collect at site of platelet plug
describe and discuss fibrous organization
clot retraction and clot destruction. activation of lytic enzymes to break up clot and restore normal blood flow through healed vessel
thrombosis
formation of a clot, usually w/i lumen of vessel (can be arterial or venous)
embolus
an unattached thrombus fragment
atherosclerosis
pathologic deposition of lipids and smooth muscle proliferation inside an artery
infarction
dead tissue, can be caused by ischemia due to thrombosis that completely blocks lumen of blood vessel
petechiae
red-purple, non-blanchable discoloration less than 0.5cm in diameter (small purpura), caused by intravascular defects, infection
purpura
red-purple, non-blanchable discoloration larger than 0.5cm in diameter (large petechiae), caused by intravascular defects, inection
ecchymoses
red-purple, non-blanchable discoloration of variable size, caused by vascular wall destruction, trauma, vasculitis
vasculitis
inflammation of the vasculature
hematoma
collection of blood out of the vessels in tissues
discuss the 5 steps in the platelet activation process
- adhesion: vWB promotes platelet aggregation
- aggregation: fibrinogen bridges platelets
- spreading: platelets change shape
- granular secretion: secretion from platelets mediates plug formation
- pro-coagulant phospholipid exposure
life span of platelets
7-10 days
discuss how vWB factor and platelets interact w/ each other
platelets adhere to vWB factor via vWB factor receptors on their surface, this facilitates formation of the platelet plug in primary hemostasis.
discuss the breakdown of the fibrin clot
plasminogen is activated to plasmin (a bunch of factors act to do this), plasmin cleaves fibrin into fibrin degredation products, clot breaks down via fibrinolysis
discuss the conversion of prothrombin to thrombin
prothrombin circulates in plasma, exposed TF activates prothrombin to thrombin. thrombin in turn activates fibrinogen into fibrin to create clot.
discuss the conversion of fibrinogen to fibrin
fibrinogen is cleaved into fibrin by thrombin.
discuss the role of thrombin in clot formation
fibrin binds platelets to help them change conformation. platelet plug forms by bridging of platelets via fibrinogen. thrombin also activates fibrinogen to fibrin to form the final product, a clot.
intrinsic pathway
platelet factor pathway, activated by trauma inside vascular system, causes platelet factors to be released, slower than extrinsic pathway.
extrinsic pathway
initiates the coag. cascade in vivo. TF is expressed on damaged endothelial cells of blood vessels, this initiates cascade of clotting factors. faster than intrinsic pathway.
common pathway
convergence of intrinsic and extrinsic pathways, ultimately leads to formation of a fibrin clot.
vitamin K is important for formation of which proteins?
- prothrombin
- factors VII, IX, X
- protein C
what are two effects of vitamin K deficiency on clotting?
- affects intrinsic and extrinsic pathways
2. causes increased PT and PTT
what are the 3 types of hemophilia we have studied?
hemophilia a: factor VIII deficiency
hemophilia b: factor IX deficiency
vWB disease: impaired platelet aggregation
what are the clinical S/S of vWB disease?
muco-cutaneous bleeding. petechiae and easy bruising, most common cause of elevated PTT
DVT
deep vein thrombosis, thrombus occurs in deep lower extremity vein, has potential to detach and become embolus
pulmonary embolism
embolus migrates to pulmonary artery and become lodged there
thrombocytopenia
abnormal decrease in platelets, may results in excessive bleeding
disseminated intravascular coagulation
clotting condition, activation of both pathways causes small clots develop in blood stream and block vessels, depletes platelets and clotting factors, can lead to excessive bleeding.
bleeding time
cause small cuts in pt. under BP cuff that is inflated on upper arm, blotted every 30 seconds
platelet count
part of CBC, normal range ~150,000-300,000/microleter
PTT
partial thromboplastin time, clotting time in seconds, measures intrinsic pathway, good test for monitoring heparin therapy
PT
prothrombin time, clotting time in seconds, measures extrinsic pathway, good for monitoring warfarin therapy
D-dimer
detects presence of d-dimer (fibrin degradation product), positive results may indicate presence of thrombus (e.g. DVT or PE)
platelet function test
determines 3 things:
- platelet ability to aggregate
- strength of blot
- responsiveness of platelets to chemotactic signals
useful in diagnosing thrombotic deficiencies (e.g. vWB disease)
what factors are involved in the intrinsic pathway
VIII, IX, X, XI, XII
what factors are involved in the extrinsic pathway
VII
describe how TFPI works to limit clot extension
targets factor VIIa-TF complex, inhibits extrinsic pathway
describe how antithrombin works to limit clot extension
targets heparin and endogenous glycoconjugates, inhibits factors VIIa, IXa, XIa, and thrombin
describe how activated protein C works to limit clot extension
targets factor V and VIII, inhibits formation of factor Xa and thrombin
describe how plasmin works to limit clot extension
targets fibrin, causes fibrinolysis to occur
factor V leiden
genetic mutation, increases pathogenic clot formation by 5-7x if heterozygous, 80x if homozygous, often goes undiagnosed. OCP, infection, smoking, surgery contribute to risk of developing a clot w/ this condition.
