Hematology Flashcards
Extrinsic pathway activation
“TF pathway”
- Starts with injury outside the vessel wall
- Organ trauma, crush injury
Extrinsic pathway factors
III, VII
Inhibited eventually to activate more by TF pathway inhibitor
“You can buy the extrinsic pathway for 37 cents”
Intrinsic pathway activation
- Damage to blood vessels
- Initiated by high molecular weight kininogen (HMWK) and activation of XII
Factor IV
Calcium
Intrinsic pathway factors
Initiated by HMWK and aXII with help of IV (calcium)
-XII, XI, IX, VIII
“You can’t get the intrinsic pathway for $12, but you can get it for $11.98”
Thrombin (in coagulation pathways)
Assists in activating V, VIII, I, XIII
- Influences platelet recruitment
- Activates adequate fibrin to clot
Common pathway
aX activated II with help from V and Ca2+
-IIa (thrombin) -> I (fibrinogen) to Ia (fibrin)
-XIII secures platelet plus with Ia
“You can get the common pathway at the five (V) and dime (10) for $1 or $2 on the 13th of every month”
Factors dependent on vitamin K
II, VII, IX, X
Cell based coagulation theory phases
Initiation
Amplification
Propagation
Factor II vs IIa
II: Prothrombin
IIa: Thrombin
Factor III
Tissue Factor
Factor I vs Ia
I: Fibrinogen
Ia: Fibrin
Cell-based theory initiation phase
- Endothelial surface is injured
- TF exposed
- Endothelial surface is less repellant to platelets
- Sub endothelial anticoagulation is down regulated
- Platelets are recruited, VII -> VIIa
- Intrinsic and common pathways activated -> Xa and IXa
- Factors X and V form complex to generate a small amount of thrombin for clot (TF pathway inhibitor limits the amount of TF)
- IX attaches to activated platelet -> VIIIa -> Xa, more thrombin is produced
- Injury perpetuates, TF is expressed, platelets mobilize to injury site
Cell-based theory amplification phase
- Thrombin generation gains momentum and acceleration
- Thrombin activated V, VIII, IX
- XIa assists in generating more IX on platelet surface
- vWF promotes platelet aggregation with Gp1b
- Platelet surface (GpIIb-IIIa) facilitates aggregation
Cell-based theory propagation phase
- All coagulation factors are actively influencing one another, promoting coagulation, activating prothrombin -> larger bursts of thrombin
- Enough thrombin needs to be present to convert fibrinogen to fibrin to form a stable secondary hemostatic plug