Coags Flashcards
what is normal hemostasis
a balance between clot generation, thrombus formation, and counter-regulatory mechanisms that inhibit uncontrolled thrombogenesis or premature thrombus degradation
what are the 3 goals of hemostasis
- to limit blood loss from vascular injury
- maintain intravascular blood flow
- promtoe revascularization after thrombosis
what are the 2 stages of hemostasis
primary hemostasis and secondary hemostasis
what is primary hemostasis
immediate platelet deposition at hte endovascualr injury site
* leads to the intial platelet plug
only adequate for minor injury
what is secondary hemostasis
clotting actors activated
stabilized clot formed and secured with crosslinked fibrin
what is a characteristic of vascular endothelial cells
they have antiplatelet, anticoagulant, and profibrinolytic effects that inhibit clot formation
anti-clotting mechanisms of the endothelial cell
is the enothelial cell negative or positively charged
negatively charged to repel platelets
anti-clotting mechanisms of the endothelial cell
what is produced by the endothelial cell
prodcue platelet inhibtors such as prostacylin and nitric oxide
what is released by vascular endothelial cells and what does it do
excrete adenosine diposphotase, which degreades adenosine diphosphate (ADP) a platelet activator
what anticoagulant is increased through the endothelial cells
increase protein C, an anticoagulant,
the endothelial cell produces tissue factor pathway inhibitor (TFPI) which inhibits what
factor Xa and TF-VIIa complex
what is synthesized by the endothelial cells
tissue plasminogen activator (t-PA)
platelets play a critical role in hemostasis, where are they derived from
bone- marrow megakarocytes
what is the lifespan of non-activated platelets
nonactivated platelets circulate as discoid anuclear cells with a lifespan of 8 to 12 years
approximately 10% of platelets are consumeed to support vascular integrity how many platelets are formed daily
1.2-1.5 x 10^11 formed daily
damage to the endothelium exposed the underlying
extracellular matrix (ECM)
the extracellular matrix contains
collagen, vWF, and other platelet adhesive glycoproteins
upon exposure to ECM platelets undergo what 3 phases of alteration
bonus: what stage of hemostasis is this
adhesion, activation, aggregation
when does adhesion occur
when exposed to ECM proteins
activation of platelets happens when the platelets are stimulated and interacts with
collagen and tissue factor (TF) causing the release of granular contents
platelets contain 2 type of storage granules what are they
alpha granules and dense bodies
alpha granules contain what
fibrinogen, factors V and VIII, vWF, plt-derived growth factor and more
what do the dense bodies contain
ADP, ATP, calcium, serotonin, histmaine, and epinphrine
aggregation occurs when
the granular contents are released, which recruits and activates additional platelets, propagating plasma-mediated coagulation
activated glycoprotein 2B/3A on the platelet surface bind what
fibrinogen, promoting fibrin crosslinking
each stage of the cascade requires assembly of the membrane activation tenase complexes
what is each complex composed of
a substrate (inactive precursor)
an ezyme (activated coagulation factor)
a cofactor (accelerator or catalyst)
calcium
Clotting Factors
Factor I is also called
fibrinogen
Factor II is also called
prothrombin
Factor III is also called
tissue thomboplastin
Factor IV is also called
calcium ions
Factor V is also called
labile factor
Factor VII is also called
stable factor
Factor VIII is also called
antihemophilic factor
Factor IX is also called
christmas factor, plasma thomboplastic component (PTC)
Factor X is also called
stuart-prower factor
Factor XI is also called
plasma thromboplastin antecedent (PTA)
Factor XII is also called
hageman factor
Factor XIII is also called
fibrin stabilizing factor
extrinisc pathway is the intiation of
plasma mediated hemostasis
what begins the extrinsic pathway
endothelial injury, exposing TF to plasma
what is the extrinisc pathway
TF forms an active complex VIIa (TF/VIIa complex)
TF/VIIa complex binds to and activates factor X converting it to Xa
TF/VIIa complex also activates IX to IXa in the the intrinsic pathway
what is needed to convert Factor X to Xa
IXa and calcium
what begins the final common pathway
factor Xa
what begins the intrinsic pathway
XIIa
most thrombotic events follow ______ pathway; however lab-coag studies rely on ____ pathway to activate the cascade
extrinsic ; intrinsic
the intrinsic pathway plays a ____ role in the initiation of hemostasis, and is more an ______ _______ system to progoate thombin generation intiated by the extrinisic pathway
minor; amplification system
upon contact with a ______ charged surface, factor ______ is activated
negatively charged ; factor XII
factor XIIa converts
XI to XIa
what converts factor X to Xa
XIa + VIIIa + platelet membrane phospholipid + Calcium
activated thrombin IIa activates which factors to amplify extrinisc thombin generation
V, VIII, XII
this process activates platelets leading to the propogation of the FCP
Factor X becomes Xa and binds with what to form prothrombinase complex
Va
p
prothrombinase complex rapidly converts
prothrombin (II) into thrombin (IIa)
thrombin attaches to platelets and converts
fibrinogen (I) to fibrin (Ia)
fibrin molecules _____ to form a mesh that stabilizes the clot
crosslink
whats happening
Vascular injury exposes TF, initiating extrinsic pathway. Intrinsic pathway further amplifies thrombin & fibrin generation. Platelets adhere to collagen, become activated, and recruit additional platelets.
thrombin cleaves fibrinopeptides A & B from fibringogen to generate fibrin monomers, which does what
polymerize into fibrin strands to form basic clot
what factor cross links the fibrin strands to stabilize and make the clot insoluble, resitant to fibrinolytic degradation
XIIIa
T/F only the intrinsic tenase complex factilitates the fromation of prothrominase complexes
false both intrinsic and extrinsic tenase complexes factilitate the formation of prothrombinase complexes