Exam 4 - Weber Hockerman Campbell Thurman Flashcards

1
Q

platelets derive from __________

A

megakaryotes

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2
Q

platelets have no _________

A

nucleus or genes

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3
Q

what are the three steps of platelet formation?

A

adhesion, secretion, aggregation

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4
Q

platelets: adhesion is mediated by:

A
  • GP Ia binding to collagen
  • GP Ib binding to vWF bridged to collagen
  • shape changes facilitates receptor binding
  • intact endothelial cells secrete PGI2 (prostacyclin) to inhibit thrombogenesis)
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5
Q

platelets: secretion release reaction

A
  • degranulation
  • platelet granules release ADP, 5-HT, TXA2
  • these molecules activate and recruit other platelets
  • TXA2 and 5HT are potent vasoconstrictors
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6
Q

what molecules are released from platelet granules

A

ADP, TXA2, 5-HT

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7
Q

which molecules released from platelets are potent vasoconstrictors

A

TXA and 5-HT

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8
Q

platelet aggregation steps

A
  • ADP, 5-HT, TXA2 activation induces conformation of GPIIb/IIIa receptors to bind fibrinogen
  • platelets are crossed-linked by fibrogen
  • forms temporary hemostatic plug
  • platelets contract to form irreversible fused mass
  • fibrin stabilizes and anchors aggregated platelets
  • forms surface for clot formation
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9
Q

what does GPIIb/IIIa bind to?

A

fibrinogen

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10
Q

platelets are _______ by fibrinogen

A

cross-linked

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11
Q

COX-1 inhibitors MOA

A

irreversible inhibition of TXA2 synthesis in platelets

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12
Q

aspirin use leads to a _______ loss of platelet COX1 activity

A

permanent

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13
Q

indications of aspirin

A

prophylaxis and treatment of arterial thromboembolic disorders

  • prevents coronary thrombosis in unstable angina
  • adjunct to thrombolytic therapy
  • reducing recurrence of thrombotic stroke
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14
Q

clinical actions of aspirin

A
  • prolongs bleeding time but no increase in PT time
  • hemostasis returns to normal 36 hours after last dose
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15
Q

side effects of aspirin

A
  • upper GI bleeding
  • aspirin overdose
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16
Q

why do selective COX inhibitors cause increased CV risk

A

selective COX2 inhibitors block synthesis of prostacyclin while not preventing the synthesis of TXA2 (increased risk of clotting)

17
Q

ADP RIs: P2Y1s couple to which pathway

A

Gq - PLC - IP3 - Ca2+ - pathway

18
Q

ADP RIs: P2Y12s couple to which pathway

A

G1 and inhibition of adenylyl cyclase

19
Q

activation of both P2Y1 and P2Y12 receptors is not required for platelet activation by ADP

A

false

20
Q

Name the P2Y12 ADP Receptor inhibitor

A

clopidogrel (plavix)

21
Q

MOA of clopidogrel (plavix)

A

irreversibly block ADP receptor on plateelt and subsequent activation of GP IIb/IIIa

22
Q

duration of action of clopidogrel after d/c

A

several days after last dose

23
Q
A