Primary Hemostasis Flashcards

1
Q

What is primary hemostasis?

A

formation of a weak platelet plug.

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2
Q

What is secondary hemostasis?

A

Stabilization of the platelet plug, mediated by the coagulation cascade.

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3
Q

What are the four steps of primary hemostasis?

A
  1. Transient vasoconstriction (endothelin)
  2. Platelet adhesion to damaged wall
  3. Platelet degranulation
  4. Platelet aggregation
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4
Q

What does vWF bind to?

A

exposed subendothelial collagen

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5
Q

How does the platelet bind vWF?

A

GP 1b receptor

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6
Q

Where is vWF stored?

A

endothelium- Weibel-Palade bodies

alpha granules of platelets

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7
Q

Describe platelet degranulation?

A

ADP release from dense granules promotes exposure of GP IIb. TXA2 (COX) promotes aggregation (next step)

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8
Q

What molecule crosslinks GPIIb receptors

A

fibrinogen

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9
Q

What is the most common cause of thrombocytopenia?

A

ITP. Immune thrombocytopenic purpura

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10
Q

In ITP IgG targets what receptor?

A

GP IIb

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11
Q

What are the lab findings in ITP?

A

decreased platelet count
Normal PT/PTT (secondary hemostasis unaffected)
increased megokaryocytes

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12
Q

What are two microangiopathic hemolytic anemias?

A

TTP. Thrombotic thrombocytopenic purpura

HUS. Hemolytic uremic syndrome

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13
Q

What is the pathogenesis of TTP?

A

Decreased ADAMTS13 leaves uncleaved multimers of vWF leading to abnormal platelet adhesion. Usually due to an autoantibody. Most commonly seen in adult females.

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14
Q

What causes HUS?

A

E coli O157:H7, usually in children

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15
Q

What are the lab findings of microangiopathic hemolytic anemias?

A
Thrombocytopenia
Increased bleeding time
Normal PT/PTT
Anemia with schistocytes
increased megokaryocytes
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16
Q

What are the qualitative platelet disorders?

A

Bernard Soulier Syndrome (genetic GP Ib deficiency)
Glanzmann Thrombasthenia (genetic PGIIb deficiency)
Aspirin irreversibly inhibits COX (TXA2)
Uremia