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Cardiovascular System > Platelet Biochemistry > Flashcards

Platelet Biochemistry Flashcards

1
Q

What do platelets come together to form

A

A thrombus

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2
Q

What is atherogenesis

A

Build up of atherosclerotic plaque in the arterial wall

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3
Q

What happens in the blood vessels as age increases

A

As age increases the more common it becomes for atherosclerotic Plaque to build up and cause the vessel to erode or rupture

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4
Q

What is the first stage of atherosclerotic plaque build up

A

Fatty streaks

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5
Q

How does a breach in the vessel wall close

A

By platelets adhering and forming a clot

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6
Q

The first stages of atherosclerotic plaque build up are silent but what do they cause in the later stages

A

The build up can cause serious conditions such as
Myocardial infarction
Ischemia
Stoke
Sudden death

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7
Q

What are platelets

A

They are cell fragments which drive haemostasis

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8
Q

When platelets are activated due to a breach in the vessel what happens to the platelet

A

They undergo a shape change from smooth discoid to spiculated and pseudopodia with finger like projections

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9
Q

Why does the platelet need finger like projections when activated

A

They increase the surface area and the possibility to make cell-cell interactions with other platelets and also other cells such as those in the sub endothelial and white blood cells

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10
Q

What receptor is on the surface of platelets

A

Glycoprotein IIb/IIIa

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11
Q

What is glycoprotein IIb/IIIa also known as

A

Intergrin protein
Alpha IIb Beta 3

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12
Q

Approximately how many receptors are on the surface of a resting platelet

A

Between 50,000 and 100,000

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13
Q

What happens to the platelets once activated

A

The number of receptors increases on the platelet surface
The affinity for fibrinogen increases

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14
Q

What role does fibrinogen play in thrombosis

A

Fibrinogen is a plasma protein that links the platelets to each other via receptors on there surface which allows platelets to bind and aggregate

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15
Q

Aggregated platelets form….

A

Aggregated platelets bind via cross linking with fibrinogen to form a mass over the breach in the vessel

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16
Q

When the atherosclerotic plaque ruptures what becomes exposed

A

The sub endothelial tissue

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17
Q

Characteristics of the endothelial tissues which stops thrombus forming

A

Smooth

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18
Q

When the sub endothelial is exposed what does this trigger

A

It triggers the response of platelet activation

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19
Q

When the sub endothelial tissue is exposed what is exposed

A

Collagen
Von willebrand factors
Soluble agonists

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20
Q

What binds with collagen in the sub endothelial tissue

A

Platelets have a collagen receptor on there surface to allow for binding when exposed

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21
Q

What does Von willebrand factor bind with in the sub endothelial tissue

A

The glycoprotein IIb/IIIa receptor on the surface of the platelet binds to the Von willebrand factor in the sub endothelial tissue

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22
Q

What role do soluble agonists play in the sub endothelial tissue

A

They activate platelets

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23
Q

What does the endothelial mono layer do in the blood vessel

A

It keeps the blood flowing and separates the blood from touching the sub endothelial tissue

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24
Q

When a platelet is activated what does this cause

A

Shape change
Cross-linking of GPIIb/IIIa
Platelet aggregation

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25
Q

What does the glycoprotein VI receptor bind to

A

Binds to collegen to activate the platelet

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26
Q

When a platelet is activated what does it activate

A

The platelet activated the GPIIb/IIIa receptors

27
Q

What happens when the GPIIb/IIIa receptor is activated

A

Allows binding of fibrinogen and allows cross linking which leads to platelet aggregation

28
Q

When the platelets bind to the the collagen through GPVI what does this cause

A

This causes platelets to synthesise and release thromboxane A2

29
Q

What is thormboxane A2

A

This is an amplification pathway to amplify the amount of platelets activated

30
Q

What does Thromboxane A2 bind to and what does it result in

A

Binds to the TPalpha receptor on the platelet surface to further activate platelets and activation of new platelets just arriving at the breach

31
Q

What is the target of aspirin

A

Aspirin inhibits the Amplification pathway of Thomboxane A2

32
Q

What is aspirin

A

The oldest anti-platelet drug

33
Q

What is Arachindonic Acid

A

This is what is converted by COX enzymes to Prostaglandin H2

34
Q

In a platelet what is prostaglandin H2 converted into and what does it lead to

A

Thromboxane A2
This leads to platelet amplification and aggregation and vasoconstriction to limit blood flow through the vessel

35
Q

In endothelial cells what is arachidonic acid converted by

A

COX-1
COX-2

36
Q

What does the prostaglandins in endothelial cells lead to

A

In endothelial cells prostaglandin H2 is converted into prostacyclin

37
Q

What does prostacyclin result in in endothelial cells

A

Prostacyclin inhibits platelet aggregation and vasoconstriction meaning it would be a vasodilator which would increase blood flow through the vessel

38
Q

What does low dose aspirin act upon in platelets

A

Low dose aspirin would act upon the COX-1 enzyme which would inhibit the production of prostaglandin H2 which would inhibit the production of Thomboxane A2 and stop platelet amplification

39
Q

Does low dose aspirin have an affect on endothelial cells

A

Limited effect as most of it would be used in the inhibition of COX-1 in the platelet that it wouldn’t reach endothelial cells and so the overall effect would be the inhibition of platelet aggregation

40
Q

What affect would high dose aspirin have

A

High dose aspirin would inhibit both COX-1 and COX-2 in both platelets and endothelial cells meaning the production of prostaglandin H2 would stop nor only inhibiting platelet aggregation but also inflammatory pathways

41
Q

What are platelet purinergic receptors

A

They are the P2Y receptors, which are G-protein coupled receptors which signals to intracellular pathways which are activated by adenine nucleotides mainly ADP

42
Q

What P2Y receptors are found on the platelet surface and what glycoprotein is it linked to

A

P2Y 1 which is linked to the Gq protein
P2Y 12 which is linked to the Gi protein

43
Q

What happens to ADP when released outside the cell in relation to P2Y 1 receptor

A

They become signalling molecules which binds to the P2Y 1 receptors on the platelet surface and activates it

44
Q

When ADP binds to the P2Y 1 receptor what does this trigger

A

This activated the platelet through the pathway phospholipase C which triggers the release of Calcium from intra cellular stores and activates the protein kinase C pathway which all initiates the process of platelet aggregation and the shape change of the platelet.

45
Q

What happens when ADP binds to P2Y 12 receptor on the surface of the platelet

A

ADP binds to P2Y 12 and activates the Gi protein on the inside of the plate late with inhibits adenylate cyclase which inhibits the production of the signalling molecule cyclic AMP which leads to the signalling and activation of other pathways. The activation of the Gi pathway also activates the enzyme pathway PI3 kinase which together amplifies platelet activation, aggregation response and the release of granules

46
Q

Describe ADP induced platelet aggregation

A

ADP binds to the P2Y1 receptor on the surface of the platelet causing platelet activation. When the platelet becomes activated the glycoprotein IIb/IIIa receptor is activated causing the fibrinogen to bind and the cross-linking of platelets so they stick together and are able to seal the breach in the vessel wall.

ADP then also binds with P2Y12 receptor on the surface of the platelet, this is an amplification pathway. This amplifies the whole response due to the activation of P2Y1 been relatively weak so adding in the activation of P2Y12 allows for a bigger and more sustained response to the breach.

47
Q

Where does the ADP that binds to the P2Y receptors on the platelet surface come from

A

The ADP is actually released from inside the platelet.
The ADP come from the dense granules inside the platelet, which are released when the platelet is activated.

48
Q

What is outside in signalling

A

This is a amplification pathway through Glycoprotein IIb/IIIa receptor.

49
Q

What does thrombin bind to on the platelet surface

A

Thrombin binds to the PAR-1 receptor on the platelet surface

50
Q

What does the binding of Thrombin with the PAR-1 receptor cause

A

This activates the platelet and aids the release of dense granules

51
Q

How is thrombin created

A

Through the coagulation cascade

52
Q

How do platelets aid the coagulation cascade and the release of thrombin

A

Platelets contribute to the coagulation cascade by creating a surface for the coagulation cascade proteins to attach to which is known as platelet procoagulant activity

53
Q

Describe the resting state in platelet procoagulation activity

A

In the resting state there are aminophospholipids on the inner surface of the platelets so they aren’t expressed on the outer surface of the membrane, and this is kept the same through a process called translocase which is an enzyme in the lipid belayer which flips the aminophospholipids so that they are on the inner surface.

54
Q

Describe what happens when the platelet coagulant activity is activated by the likes of thrombin on the PAR-1 receptor

A

When thrombin activates the PAR-1 receptor on the outside of the platelet, calcium is trigger to release from the intracelluar stores which is a signalling molecule within the cell. The calcium release is part of the activation process in platelets, the calcium inhibits the enzyme translocase and activates the enzyme scramblase. This enzyme breaks down the asymmetry in the phospholipid bilayer, which causes the flipping of the aminophospholipids to the external of the bilayer. This means they become expressed and allow them assembly of some of the coagulation cascade proteins so prothrombin and become thrombin through the prothrombinase complex (factor Va and factor Xa)

55
Q

How does platelet procoagulant activity link to the increase in platelet activation

A

Thrombin activates the PAR-1 receptor which increases the release of intracellular calcium which causes the translocase enzyme to be inhibited and the scramblase enzyme to be activated flipping the aminophospholipids to the external of the bilayer where the prothrombase complex can bind and turn prothrombin into thrombin which is then released from the platelet and binds with the PAR-1 and PAR-4 receptors on the platelet surface to amplify the platelet aggregation

56
Q

What is a platelet-fibrin clot, how does it form and why is it important

A

Due to the relationship between thrombin and the coagulation cascade, platelet-fibrin clots form. Platelets aggregate together along with red cells clumped together within a mesh o fibrin strands which formed due to thrombin cleaving fibrinogen into fibrin, which binds the clot together and stabilises the clot.

57
Q

Why is it important that the clot contains the fibrin stands to stabilise it

A

This is important because when a fibrin Rich clot has formed it is really hard for the body to breakdown without activating the fibrinolytic system.

58
Q

How does the fibrinolytic system work

A

Tissue plasminogen activator is release from the endothelium which converts the plasma protein plasminogen into plasmin. The plasmin is then used to break down the fibrin stands into degradation products

59
Q

What inhibits tissue plasminogen activator

A

PAI-1/ plasminogen activator inhibitor-1

60
Q

What inhibits plasmin

A

Anti plasmin complex inhibits plasmin

61
Q

What are alpha granules in platelets

A

Play a role in Inflammation and healing.

62
Q

When does the platelet release alpha granules

A

They begin to release alpha granules when the platelet becomes activated through any of the pathways.

63
Q

What do alpha granules contain

A

Coagulation factors and inflammatory mediators

64
Q

What is the role platelets have in inflammation

A

They do this through the expression of P-selectin which is bound to the inside surface of the alpha granules which then are released and fuse to the external membrane of the platelet. The counter receptor for P-selection is found on the surface of leukocytes and monocytes, which is PSGL-1. This allows the platelet to bind to the leukocyte or monocyte in question. Thus leads to cross talk between the cell and the platelet which can lead to a thrombotic response and increases the inflammatory response which can help with wound healing

Cardiovascular System (12 decks)

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