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Lecture 4: Primary Hemostasis
Terms in this set (22)
What 3 tests can measure primary hemostasis?
Bleeding Time (Not performed anymore)
Platelet Function Tests
Platelet Aggregation Tests
Function of vWF? What site does it bind to on platelets?
Binds to PLT site GP Ib/IX/V
Main function is to carry factor VIII and is the bridge between PLTs and damaged tissue.
What is the PLT receptor for vWF?
In plasma, vWF binds to collagen, PLTS then attach to vWF via GP Ib/IX receptor
Which are the 3 non platelet source agonist? Their Strength?
Collagen and Thrombin are strong
Epinephrine is weak
Which are the 4 platelet source agonist? Why are they all weak in strength?
ADP, Serotonin, TA2, Platelet-activating factor (PAF)
If these were strong they could activate by themselves, being weak means they need extra help.
Function of G Proteins
Many agonists are tied to G proteins, they act as switches to inactivate/activate enzyme reactions.
Function of Phospholipase C (PLC) PW:
G proteins activate PLC, which in turn releases IP3 (Releases Ca 2+ from DTS) and DAG (Triggers granule secretion)
What is in charge of Ca 2+ regulation?
Function of the cAMP pathway in PLT activation?
This PW inhibits Primary hemostasis, its a negative regulator. PGI2 (ECs) stimulates adenyl cyclase = Increase cAMP, DRP inhibits adenyl cyclase = Decrease cAMP. Therefore, less cAMP means less inhibition and easier primary hemostasis.
How does aspirin work on PLTs?
Inhibits cyclo-oxygenase of the Arachidonate PW. No cyclo-oxygenase means no TXA2 which is a PLT agonist.
Aspirin has no impact on PLT counts, just PLT function.
How does PLT shape Change impact PLT activation?
PLTs changing to Spherical rather than flat allows granules to move towards center, increases surface area for reactions, and more contact with other PLTs. This also changes the surface receptors.
What changes in the surface receptors once PLT shape is changed?
GPIb/IX is internalized and GPIIb/IIIa is brought to surface to allow PLT aggregation to occur (PLT adhesion has occurred)
What is happening during PLT aggregation?
PLTs become attached to one another due to GPIIb/IIIa exposed/activated during shape change and Fibrinogen (in circulation) binds PLT GPIIb/IIIa receptors and acts as a protein bridge between PLTs.
How does PLT secretion cause a positive feedback?
Once shape change leads to centralization of granules, they are released through OCS to exterior of PLT. Granules act as agonist to further activate PLTs
Examples of Positive feedback mechanisms in Dense granules? (2)
ADP: Increases Ca and PLT release, activates GPIIb/IIIa
Ca: Aids in fibrinogen attachment
Examples of positive feedback in alpha granules?
5. Factor V, Fibrinogen
1. Heparin neutralizing activity, chemoattractant
2. Stabilizes aggregated PLTs
3. Healing of injured Tissues
4. PLT adhesion
5. Formation of fibrin, PLT adhesion
Q break: Which of the following is NOT true regarding the consequences of platelet shape change during primary hemostasis?
a. it results in increased surface area for biochemical reactions
b. the platelet's granules become centralized
c. pseudopods allow for more contact between additional platelets and the injured tissue
d. it results in activation of GPIb/IX receptor on the surface of the platelet
It results in the activation of GPIIb/IIIa on the surface, the GP Ib/IX becomes internalized.
Q Break: Which of the following does NOT act as a platelet agonist?
b. Cyclic AMP (cAMP)
cAMP is actually a negative regulator of platelets (not an activator). It inhibits platelet shape change, secretion, and GPIIb/IIIa activation.
Q Break: What is the mode of action of aspirin?
a. it inhibits cyclo-oxygenase, leading to inhibition of Thromboxane A2
b. in inhibits thrombin
c it causes the spleen to sequester more platelets, lowering the count in the bloodstream
d. it blocks the platelet's GPIb/IX receptor
Q Break: During platelet adhesion, platelets adhere to subendothelial collagen via:
a. their own GPIIb/IIIa receptor and fibrinogen
b. their own GPIIb/IIIa receptor and vWF
c. their own GPIb/IX receptor and fibrinogen
d. their own GPIb/IX receptor and vWF
Q break: The GPIIb/IIIa platelet receptor and fibrinogen are necessary for:
a. platelet adhesion
b. platelet activation
c. platelet aggregation
d. platelet secretion
Q break: In the process of forming the primary hemostatic plug, all of the following occur during the process of platelet aggregation except?
A. Reversible primary aggregation followed by secondary aggregation which is Irreversible
B. Fibrinogen "bridges" (links together) adjacent platelet molecules
C. GPIb/IX surface receptors appear for fibrinogen attachment
D. The platelet shape changes from discoid to spiny
GPIIb/IIIa appear for fibrinogen attachment
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