hemostasis Flashcards
what is primary hemostasis
- Vasoconstriction (Immediate Response)
• When a blood vessel is injured, it constricts to reduce blood loss.
• This is triggered by endothelin, released by the damaged endothelium. - Platelet Adhesion
• The injury exposes collagen in the blood vessel wall.
• Von Willebrand Factor (vWF) binds to collagen and acts as a bridge.
• Platelets attach to vWF using the GP1b receptor. - Platelet Activation
• Bound platelets change shape and become “activated.”
• Activated platelets release granules containing:
• ADP → Increases platelet stickiness by upregulating GP2b/3a receptors.
• Thromboxane A2 (TXA2) → Promotes more platelet activation and vasoconstriction.
• Calcium (Ca²⁺) → Helps in coagulation. - Platelet Aggregation
• Activated platelets link together using fibrinogen as a bridge.
• This is mediated by the GP2b/3a receptor.
end result of coagulation cascade
converts fibrinogen to fibrin and makes a strong clot.
what converts fibrinogen to fibrin
thrombin
what are the pathways in coagulation cascade
extrinsic = TF (3) , factor 7
intrinsic = 12, 11, 9 , 8
common= 10, 5, 2, 1
extrinsic pathway
Tissue damage releases Tissue Factor (TF) → Activates Factor VII, which activates Factor X.
intrinsic pathway
Blood vessel damage exposes collagen → Activates Factor XII, leading to activation of Factors XI → IX → VIII → X.
12,11,9,8,10
factor 10 activation leads to
Factor X (Xa), with Factor V, converts Prothrombin (Factor II) → Thrombin (Factor IIa).
what factor stabilizes fibrin
factor 13
fibrinolysis process
Plasminogen Activation= Plasminogen (inactive) is converted to Plasmin (active).
tPA (Tissue Plasminogen Activator)- key enzyme
what lab test is main test in fibrinolysis
D-dimer
what inhibits thrombin
Fibrinogen/fibrin degradaAon products
where is plasminogen produced
produced by liver, circulates in plasma and gets incorporated into blood clots during their formaAon
what are primary hemostasis due to
o Vascular defects
o Thrombocytopenia
o Platelet dysfuncAon
o VWD (inherited or acquired)
what does primary hemostatis present as mucocytaneous bleeding
o Immediate and superficial
o Petechia and wet purpura (mucosa)
o Melena, hematuria
o Menorrhagia
o Epistaxis
Secondary hemostasis disorders due to:
o Inherited deficiency of coagulation factors (e.g. hemophilia)
o InhibiAon of coagulation factors
secondary hemostasis disorder present as
o Present as deep and delayed bleeding (bleeding arrests at first because hemostasis is intact, but fibrin cannot be formed, resulting in bleeding)
o Hemarthrosis
o Intramuscular, large ecchymosis (big hematomas)
APTT
It evaluates the intrinsic and common pathways of the coagulation cascade
pneumonic: plat tenis table (inside)
PT
play tenis (outside) extrinsic pathway
INR
a way of standardizing results of PT [raAo of patients PT and the normal mean PT] =to monitor anticoagulation with warfarin
thrombin test
we do not need Ca or PL because it is a direct enzyme that acts on fibrinogen immediately
what prolongs APTT and PT
• Heparin =prolongs APTT
• Warfarin =prolongs PT
how to test for platelet function test
Light transmission aggregometry
o Take plasma that is rich in platelets, add agonists that promote aggregators
o If platelets are functioning normally –>aggregate–>medium will be clear–>light will pass
o If dysfuncAonal-don’t aggregate -medium is opaque because platelets are All there -light won’t pass
normal pt and aptt
problem in primary hemostasis
platelet problem, BV problem, factor XIII problem, mild factor deficiency (not < 30%), abnormal fibrinolysis
Normal PT and abnormal APTT =mixing studies
o Corrected =deficiency of 8, 9, 11, 12 - test for these factor deficiencies o Not corrected =inhibitor
