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21 Cards in this Set
- Front
- Back
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what is the normal platelet count??
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- 150,000-400,000
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what is the surface canalicular system of platelets?
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- connects granules to inside of platelet so they can be released when it is activated
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what do you find in the alpha granules of platelets?
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- fibrinogen & thrombospondin for aggregation
- vWF to help adhere platelet to vessel - Factor V to help promote clot, PF4 is a heparin antagonist & promotes fibrin clot - beta thromboglobulin recruits fibrobasts, PDGF to recruit fibroblasts, P-selectin to adhere platelets to phagocytic cells |
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what do you find in the dense granules?
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- ADP & ATP for platelet activation & recruitment
- serotonin for vasoconstriction for promoting coagulation - calcium which is cofactor for fibrin clot formation |
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what do you find in the lysosomes?
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- hydrolytic enzymes, phagocytic debris
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what does GPIb do? GP Ia/IIa? GP IIb/IIIa? what does P-selectin do?
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- GPIb: vWF recetpro
- GPIa/IIa: collagen receptor - GP IIb/IIIa: fibrinogen receptor - P-selectin is leukocyte adhesion on activated platelets only! |
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what binds glycoprotein binds vWF? what binds collagen?
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- GP Ib binds vWF
- GP Ia/IIa bind collagen - this is the process of adhesion |
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what happens during activation? what agents are activating agents?
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- induces platelet shape change & secretion (induces shape change from sphere --> long increased surface area to allow them to stick together)
- important activation agents = thrombin & thromboxane A2 |
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what important glycoproteins & alpha granules allow platelet platelet interaction?
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- GP IIb/IIIa b/c that interacts with fibrinogen
- thrombospondin b/c that also interacts with fibrinogen - aka really need fibrinogen to bind two platelets together |
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what does the bleeding time test look at?
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- vWF (if there is enough) & if platelets are functional
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what is the light transmission aggregation platelet lab looking at?
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- use platelet rich plasma & palatelet agonists (ADP, collagen, epi, thrombin, ristocetin) --> if they aggregate & fall to bottom of tube light transmission will increase
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what does an abnormal response to ristocetin dictate?
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- if they do not aggregate means you have disruption in vWF b/c ristocetin requires vWF
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what does it mean if you see big platelets in BM? ghost platelets? clumping platelets?
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- enlarged platelets = BM reved up to make platelets rapidly
- ghost platelets = no granules - clumping platelets = trauma during getting the sample |
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what does the PFA-100 test?
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- pass the blood through a membrane with collagen or epi or ADP and then time how long it takes the membranes to close
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what are the two inherited thrombopathies?
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- bernard soulier disease: GPib (vWF receptor)
- Glanzmann's thrombasthenia: G11b/IIIa (fibrinogen receptor) |
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how does aspirin & ibuprofen cause drug induced thrombopathy?
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- ASA irreversibly & ibuprofen irreversibly inhibit COX --> decreased in thromboxane A2--> decreased vasoconstriction & aggregation
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how can cardiac bypass?
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- platelets release alpha granules & are also destroyed --> thrombocytopenia
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what is thrombocytopenia?
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- platelets <150,000
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what is allo-immunization (NAIT)?
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- antibody passed from mother --> newborn which destroys platelets, it is transient
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what is DIC? what is the most common cause? what do you see in the labs?
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- thombocytopenia, excessive fibrinolysis, reduced coagulation factors
- endotoxin most common cause - in the labs you see microangiopathic HA, prolonged PT/PTT, increased d-dimer |
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what is ITP? how do you treat? what do you see clinically?
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- autoimmune against platelet, targets it for removal via RES
- treat w/ steroids, IVIG, WinRho (soln of antibodies against red cells to block spleen) - clinically you see low platelets but BM is trying to increased platelets so will see giant ones there |
