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IHL Exam 1 Me > Platelet Function (McCormick) > Flashcards

Platelet Function (McCormick) Flashcards

1
Q

3 fundamental building blocks for clotting

A

1) Endothelium
2) Platelets
3) Coagulation (fibrin formation)

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2
Q

Injury of endothelium

A

Transient vasocontriction

Exposure of ECM

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3
Q

Endothelin

A

Released by injured endothelium

causes vasoconstriction

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4
Q

Charge of intact vessel luminal surface

A

negative
so repels the negative platelets
so no clot!

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5
Q

Blood Plasma contact with ECM during injury

A

triggers activation of physiologic clotting with platelet adhesion molecules (GPIb, integrins)
recognizing these ECM components

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6
Q

Components of extracellular matrix (ECM)

A

collagen
Fibronectin
laminin
vWF

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7
Q

vWF

A

Synthesized by endothelial cells and expressed on surface of ECM

serves as vital link for platelet adherence and activation

deficit–> platelets can’t attach

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8
Q

GP1B

A

Receptor on the platelets that attaches to vWF

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9
Q

Sources of vWF

A

1) Endothelial cells
2) megakaryocytes–> precursors of platelets
circulate in blood and carry vWF that is circulating in the blood
3) platelet alpha granules

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10
Q

vWF’s action of factor 8

A

grabs onto factor 8 circulating in the blood and activate endothelial cells to produce more active factor 8

maintains level and activity of factor 8 in the blood by increasing the t1/2 of factor 8 (so it stays in blood longer)

decrease in vWF –> decrease in factor 8 activity and levels

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11
Q

vWF factor A3 domain

A

binds to collagen of ECM

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12
Q

vWF A1 domain

A

links with platelet receptor glycoprotein (GPIb) on filopodia

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13
Q

Gp IIb/IIIa

A

Receptor located on filopodia of platelets

once platelets start changing shape this receptor is localized to the outside of platelets

very important b/c it grabs onto passing by platelets, causing aggregation

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14
Q

GpIb

A

attaching the initial platelets to underlying ECM via vWF

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15
Q

Primary homeostasis steps

A

Adhesion
Activation (changes shape too)
Aggregation

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16
Q

Fibrinogen

A

Circulates in blood and acts as a bridge between Gp IIb/IIIa on platelets filipodia for platelet aggregation

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17
Q

Von Willebrand Disease

A

Lack of vWF
lack of platelets recruited to initial site of injury

decrease in factor 8 in blood, so decrease in intrinsic pathway

normal platelet count

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18
Q

Glanzamann thrombasthenia

A

GpIIb/IIIa mutation

causes deficiency in aggregation so platelets can’t grab eachother anymore

does NOT effect platelet count or platelet morphology

must measure platelet aggregation

19
Q

Coagulation studies (Quantitative)

A

Do or do not have enough of coagulating factor or platelets

20
Q

Coagulation studies (qualitative)

A

have enough but just not working correctly

21
Q

what releases thrombin

A

platelets

22
Q

Cytoskeletal tubular element on the outside of platelet disc

A

constricts when platelet plug is formed so the platelet plug doesn’t stick out

also forms a platform (smooth) for secondary hemostasis

23
Q

Reopro (Abcizimab)

A

Block GPIIb/IIIa receptor so aggregation doesn’t happen

induces Glanzmann thrombasthenia

24
Q

Aspirin

A

Blocks cyclooxygenase pathway that produces prostaglandins (including TxA2 which is important in aggregation)

so Aspirin makes it harder for platelets to aggregate

25
Q

Tissue factor (secondary hemostasis)

A

after platelet plug is formed, this is released by adjacent endothelial cels

starts platform of platelets producing phospholipids on their surface

this activates thrombin and polymerizes fibrinogen into fibrin

26
Q

Phospholipid platform

A

formed when platelets undergo a conformation change, exposing phospholipid-rich portion of the platelet membrane

dramatically accelerates production of fibrin

27
Q

Serum

A

Whole blood allowed to clot

still contains fibrinogen

28
Q

Plasma

A

blood drawn into collection tube containing anticoagulant that prevents clotting

anticoagulation accomplished by using agent that chelates calcium

ca is essential in the coagulation cascade so if you don’t have it blood doesn’t clot

29
Q

Quantitative Platelet Count

A

Automate analyzer

30
Q

Qualitative platelet function testing

A

Aggregation studies

31
Q

Bleeding time

A

Tests for defects in primary hemostasis as well as vWF disease

Are there enough platelets and are they working properly?

Does not test coagulation factors ONLY PLATELETS

Less than 8 min, less than 5 optimal

32
Q

Increase platelet count by tapping into…

A

Circulating pool (blood)

Marginalized platelets (pulmonary veins and spleen)

33
Q

Automated Hematology analyzers

A

Meaure Mean Platelet Volume

34
Q

Mean Platelet Volume (Quantitative)

A

Tells us the size of the platelet (tests primary hemostasis)

If platelets are being put out at a greater rate, then more of them will be larger (younger, new)

So there will be an increase in MPV

Above 8.1 fL then too large!!

35
Q

Platelet aggregation studies

A

Qualitative (primary hemostasis)

used to detect functional disorders of platelets

if you do a study to see platelets aggregate, and add epinephrine, ADP, collagen, arachidonic acid (prescursor to TXA2) or thrombin, it would NOT aggregate meaning problem with platelets connecting to each other

36
Q

Testing Secondary Hemostasis

A

Coagulation

1) PT
2) aPTT

37
Q

When does secondary hemostasis occur?

A

After the initial platelet plug has been established at the site of the endothelial injury

it involves forming larger and more stable clot by making more Fibrin from the coagulation cascade

38
Q

PT

A

Prothrombin Time- measures amount of time blood takes to clot in the presence of certain factors

Test that is used to monitor defects in extrinsic pathway

Also used to monitor coagulants (like coumadin) in pt’s (such as pt’s who have atrial fibrillation)

Coumadin affects extrinsic pathway

39
Q

aPTT

A

Activated partial thromboplastin time - used to monitor defects in the intrinsic pathway

Monitors heparin (anticoagulant) therapy

Heparin affects intrinsic pathway–> prolonged aPTT (means blood takes longer to clot)

40
Q

What factors are Vitamin K dependent

A 
Prothrombin
VII (7)
IX (9)
X (10)
2 (thrombin/prothrombin)
41
Q

Platelet function

A

Adhere to vessel wall
Activate and secrete granules
Aggregate via filapodia and fibrinogen bridges to produce platelet plug
Facilitate generation of thrombin- helps fibrinogen change to fibrin
reinforce platelet plug

42
Q

Coumadin

A

affects extrinsic pathway

43
Q

Heparin

A

affects intrinsic pathway

IHL Exam 1 Me (11 decks)

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