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Biochemistry > Primary Hemostasis > Flashcards

Primary Hemostasis Flashcards

1
Q

Hemostasis

A

the cessation of bleeding at vascular injury site via the formation of a thrombus

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2
Q

A thrombus consists of what two primary components?

A
  1. Platelet Plug
  2. Fibrin Clot
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3
Q

What is Primary hemostasis?

A

Platelet Plug: Circulating platelets form a physical plug by adhering to the injury site (and each other) in order to stop the leak

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4
Q

From what are platelets produced?

A

Megakaryocytes in the bone marrow

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5
Q

Define Thrombocytopenia

A

having a platelet count less than 1x105 /mL

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6
Q

What part of platelets allows them to bind to damaged vessel walls and/or to eachother?

A

Platelets contain glyoproteins (glycosylated, integral membrane proteins) which mediate binding to collagen and von Willebrand factor

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7
Q

The glycoprotein on platelets GPIb binds to what?

A

von Willebrand factor

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8
Q

The glycoprotein on platelets GPIIb/IIIa binds to what?

A
  • von Willebrand factor
  • Fibrinogen
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9
Q

What are the two types of granules (Storage vesicles) that platelets contain? What do each store?

A
  1. Dense granules (Ca2+, ADP)
  2. Alpha granules (von Willebrand factor, fibrinogen, coagulation factor V and VIII)
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10
Q

Damage to endothelial lining results in the exposure of what two subendothelial molecules that are essential for the initial adhesion of platelets at the site of injury?

A
  • Collagen
  • von Willebrand Factor
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11
Q

What are the four relevant binding sites of vWF protein?

A
  • coagulation factor VIII
  • GPIb
  • Collagen
  • GPIIb/IIIa
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12
Q

Resting platelets initially adhere at damaged site via GPIb glycoproteins that bind to vWF. Is this interaction strong?

A

This interaction (GPIb-vWF-collagen) is fairly weak; platelets are tethered to subendothelia but are not firmly adhered?

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13
Q

How does high shear forces create a stronger adhesion between platelets and subendothelial cells?

A

High shear forces produce a conformational change in vWF that enhances its binding to GPIb

  • Therefore; increased platelet adhesion in arteries
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14
Q

Upon platelet activation, undergoes a conformation change that reveals a preveioulsy hidden binding site for .

A
  • GPIIb/IIIa
  • vWF or fibrinogen
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15
Q

What process begins Primary Aggregation of Platelets to Subendothelial cells at injury site?

A

Activated GPIIb/IIIa binds to vWF at subendothelial surface to promote strong adhesion to the vessel wall

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16
Q

Activated platelets synthesis and secrete what in Secondary Activation?

A
  • TXA2
  • ADP
  • These two Platelet Agonists activate other resting platelets
17
Q

How do the platelet agonists (ADP, Thrombin, TXA2 stimulate activation of resting platelets?

A
  1. Each agonist binds to its specific Gq-linked receptor
  2. Via Gq-mediated signaling, an increase in cytosolic Ca2+ occurs
  3. Calcium leads to the activated on PLA2
  4. PLA2 hydrolyzed membrane phospholipids leading to production of TXA(1-3)
18
Q

What is the significance of GPIIb/IIIa molecules on platelets binding to fibrinogen?

A

Secondary Aggregation: One fibrinogen molecule can be bound by TWO GPIIb/IIIa molecules (from adjacent platelets) allows fibrinogen to secure platelets together

19
Q

In healthy vasculature, cirulating platelets are maintained in an INACTIVE state by endothelia in what 3 ways?

A
  1. Endothelial cells secrete Nitric Oxide: inhibits platelet aggregation and promotes vasodilation
  2. Endothelial cells express a membrane associated ADPase: degrades ADP that is released from activated platelets
  3. Endothelial cells release PGI2 which binds to Ga-s coupled receptor and indirectly prevents activation of phospholipase A (needed for eicosanoid synthesis)
20
Q

What is the mechanism of PGI2 in the prevention of platelet plug formation?

A
  1. Healthy Endothelia secrete PGI2
  2. PGI2 binds to Gs-linked membrane receptor on platelet
  3. Increase in cAMP and PKA
  4. cAMP activates calcium pump that actively transports calcium from from the cytoplasm
  5. Decrease in cytosolic Ca2+ prevents Ca2+ activation of PLA2
  6. No PLA2 means synthesis of TXA2 in inhibited
21
Q

What is the mechanism of action of Aspirin?

A
  • COX enzyme inhibitor -> decreased TXA2 synthesis
  • Decreased platelet activation and degranulation
22
Q

What is the mechanism of action of Plavix?

A
  • ADP-receptor inhibitor
  • Decreased ADP-mediated secondary activation
23
Q

What is the mechanism of action of Abciximab (Reopro)

A

Inhibit GPIIb/IIIa interaction -> decreased platelet aggregation

24
Q

What is the mechanism of action of Dipyridamole?

A
  • PGI2 agonist
  • Inhibits phosphodiesterase that breaks down cAMP
  • (inc. cAMP → dec. cytosolic Ca2+ → dec. PLA2 activity and thrombosis)
25
Q

von-Willebrand Disease

  • Platelet defect?
  • Platelet function affected?
A
  1. Defective or deficient von Willebrand factor
  2. Adhesion to vWF, primary aggregation (GPIIb/IIIa); Factor VIII (half-life was prolonged by vWF)
26
Q

Thrombotic Thrombocytopenic Purpura

  1. Platelet defect?
  2. Platelet function affected?
A
  1. Mutation of ADAMTS13 results in high levels of high molecular weight vWF
  2. Exaggerated thrombosis (increased platelet plug formation)
  3. Thrombocytopenia (due to abnormally high use of platelets to form microthrombi)
27
Q

Bernard-Soulier Syndrome (Giant Platelet syndrome)

  1. Platelet defect
  2. Platelet function affected
A
  1. Defect or deficiency of GPIb
  2. Adhesion to vWF
  3. Prolonged bleeding time
28
Q

Idiopathic Thrombocytopenic Purpura

  1. Platelet defect
  2. Platelet function affected
A
  1. Immune response against GPIb or GPIIb/IIIa
  2. Platelets are destroyed by cells of the immune system
  3. Severe Thrombocytopenia
  4. Facilitate platelet degradation by macrophages in spleen → SPLENOMEGALY
29
Q

Glanzmann Thrombasthenia

  1. Platelet Defect
  2. Platelet Function affected
A
  1. Defect or defiency of GPIIb/GPIIIa
  2. Primary aggregation (binding to vWF)
  3. Secondary aggregation (binding to fibrinogen)

Biochemistry (7 decks)

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