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Biochem 2 > Platelets, von Willebrand factor > Flashcards

Platelets, von Willebrand factor Flashcards

1
Q

Arterial thrombi are also rich in ___

A

platelets

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2
Q

Is Arterial thrombi platelet-dependent or thrombin-dependent?

A

Platelet-dependent

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3
Q

Is Venous thrombosis platelet-dependent or thrombin-dependent?

A

Thrombin-dependent

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4
Q

What is Margination?

A

high number of platelets by the wall, fast flow and red blood cells needed (normal hematocryt!)

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5
Q

What are Platelets?

A

small, non-deformable cells, which are pushed against the wall by red blood cells flowing in the main stream – margination

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6
Q

What is happening here?

A
  1. Primary adhesion
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7
Q

Collagen receptors on platelets
-> What is the role of GpIaIIa?

A

integrin, inactive on resting platelets

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8
Q

Collagen receptors on platelets
-> Characteristics of GpVI

A

Ig-type receptor, does not withstand shear

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9
Q

Collagen receptors on platelets
-> At high shear, what is necessary?

A

At high shear the collagen-von Willebrand factor- GpIb is necessary

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10
Q

Collagen receptors on platelets
-> Is GpIb functional even in resting platelets?

A

At high shear the collagen-von Willebrand factor- GpIb is necessary

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11
Q

Where is von Willebrand Factor synthesized and stored?

A

Endothelial cells synthesize and store it in Weibel-Palade bodies

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12
Q

Describe Structure of von Willebrand Factor – modular structure

A

In globular conformation: only the collagen-binding site in A3 is accessible

Platelet-binding sites (GpIb, GpIIbIIIa), and ADAMTS13-cleavage sites (VWF-cleaving metalloprotease) are hidden

FVIII-binding prolongs the life-time of FVIII in blood

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13
Q

Does A GpIb-Receptor recognize the globular VWF circulating in plasma? Why?

A

A GpIb-Receptor does not recognize the globular VWF circulating in plasma, only if its unfolded upon shear forces – ultralarge, or immobilized on collagen

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14
Q

Characteristics of Platelet activation

A

-i.c.Ca2+↑
-Integrin-aktivation
-secretion of granules(ADP, TXA2)

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15
Q

Platelet adhesion, activation and aggregation
-> What is happening here?

A
  1. secretion: ADP, TromboxánA2, (Serotonin), P-Selectin
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16
Q

Platelet adhesion, activation and aggregation
2. secretion: ADP, TromboxánA2, (Serotonin), P-Selectin
-> Activation: release of granules
-> What happen when releasing gamma-granules?

A
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17
Q

Platelet adhesion, activation and aggregation
2. secretion: ADP, TromboxánA2, (Serotonin), P-Selectin
-> Activation: release of granules
-> What happen when releasing alpha-granules?

A
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18
Q

Platelet adhesion, activation and aggregation
2. secretion: ADP, TromboxánA2, (Serotonin), P-Selectin
-> Activation: synthesis and release of TXA2 (in case of EICOSANOIDs: lipid mediators)

A
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19
Q

Platelet adhesion, activation and aggregation
2. secretion: ADP, TromboxánA2, (Serotonin), P-Selectin
-> Activation: synthesis and release of TXA2 (in case of Cyclooxygenase pathway)

A
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20
Q

What is the role of Aspirin acetylates cyclooxygenase?

A

irreversible inhibition

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21
Q

How can Aspirin acetylates cyclooxygenase cause irreversible inhibition?

A
  1. TXA2-synthesis in platelets inhibited platelet aggregation
  2. PGI2-synthesis in endothelial cells inhibited
    => Platelet aggregation inhibited

PGE2 synthesis in gastric mucosa decreases – acidic erosion, bleeding as a side-effect

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22
Q

Platelet adhesion, activation and aggregation
-> What is happening here?

A
  1. Integrin-activation: GpIIbIIIa, and GpIaIIa
23
Q

What is the structure of integrins?

A

Integrins : the activatable receptors
=> Heterodimers of alpha and beta subunits

24
Q

Describe Conformational states of the integrins

A
25
Q

What are the 3 Important integrins in hemostasis

A

Mac1 (aMb2)
GpIaIIa (aIIb1)
GpIIbIIIa (aIIbb3)

26
Q

Important integrins in hemostasis
-> The role of Mac1 (aMb2)?

A

monocytes, MACs, adhesion and
phagocytosis

27
Q

Important integrins in hemostasis
-> The role of GpIaIIa (aIIb1)?

A

collagen receptor on activated
platelets, withstands shear forces – stable adhesion

28
Q

Important integrins in hemostasis
-> The role of GpIIbIIIa (aIIbb3)?

A

on activated platelets, RGD sequence recognized, e.g. in fibrinogen, von Willebrand Factor. Important therapeutical target (GpIIbIIIa-blockers)

29
Q

Platelet adhesion, activation and aggregation
-> What is happening here?

A
  1. Stable aggregates
30
Q

What are necessary for stable aggregates?

A

GpIb and GpIIbIIIa

31
Q

GpIb and GpIIbIIIa are necessary for stable aggregates
-> What enhance their formation?

A

high fibrinogen-, VWF-concentrations

32
Q

Agonists for platelet aggregation
-> Agonist: Thrombin
-> Source?

A

Coagulation cascade

33
Q

Agonists for platelet aggregation
-> Agonist: Thrombin
-> Receptors

A

PAR-1, PAR-4, GpIba

34
Q

Agonists for platelet aggregation
-> Agonist: ADP
-> Resources?

A

Platelet delta-Granules

35
Q

Agonists for platelet aggregation
-> Agonist: ADP
-> Receptors?

A

P2Y1, P2Y12

36
Q

Agonists for platelet aggregation
-> Agonist: collagen
-> source?

A

Extracellular matrix

37
Q

Agonists for platelet aggregation
-> Agonist: collagen
-> Receptors?

A

GpIa/IIa, GpIIb/IIIa, GpVI

38
Q

Agonists for platelet aggregation
-> Agonist: Thromboxane A2
-> Source?

A

Synthesis in platelets

39
Q

Agonists for platelet aggregation
-> Agonist: Thromboxane A2
-> Receptors?

A

TxA2R

40
Q

Agonists for platelet aggregation
-> Agonist: PAF
-> Sources?

A

Leukocytes

41
Q

Agonists for platelet aggregation
-> Agonist: PAF?
-> Receptors

A

PAF-R

42
Q

Agonists for platelet aggregation
-> Agonist: Serotonin (5HT)?
-> Source?

A

Platelet delta-Granules

43
Q

Agonists for platelet aggregation
-> Agonist: Serotonin (5HT)?
-> Receptors

A

5HT2A

44
Q

Signal transduction in platelets
-> What are the factors that contribute to activation?

A

Increased Ca2+ concentration
Decreased cAMP concentration

45
Q

Signal transduction in platelets
-> What are the factors that contribute to inhibition?

A

Increased cAMP concentration

46
Q

Platelet adhesion, activation and aggregation
-> What is happening here?

A
  1. Phosphatidyl-serine on the surface: procoagulant platelets
47
Q

Phospholipids in platelet membrane
-> The intracellular Ca2+ concentration rises
-> What is the consequence?

A

i.c. Ca2+ rises, which inhibits flippase (aminophospholipid-translocase), and activates scramblase, so PS gets into the outer PL-layer – “procoagulant platelets” – assembly of activation complexes leads to a burst of thrombin generation

48
Q

Benard Soulier syndrome is a deficiency of ___

A

GpIb

49
Q

Glanzmann thrombasthenia is a deficiency of ___

A

GIIb/IIIa Receptor

50
Q

von Willebrand disease is a deficiency of ___

A

vWf

51
Q

An example of cyclooxygenase inhibitor

A

Acetyl salicylic acid

52
Q

2 examples of ADP antagonists

A

Ticlopidine
Clopidogrel

53
Q

3 examples of “glycoprotein IIb/IIIa antagonists”

A

Abciximab
Eptifibatide
Tirofiban

Biochem 2 (38 decks)

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