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Physiology & Pharmacology of Systems > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

The stopping of blood loss from damaged vessels.

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2
Q

What are the properties of platelets under normal circumstances and where are the found?

A

They are non-adhesive and are found circulating freely in the blood.

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3
Q

During vessel wall injury, what happens to the circulating platelets?

A

They become ‘sticky’ and aggregate.

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4
Q

What is thrombosis? What conditions can it lead to?

A

The formation of a blood clot inside a vessel. It can lead to MI (heart) or stroke (brain).

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5
Q

Explain why haemostasis is described as an ‘active’ process?

A

Because even arrest processes are occurring to STOP inappropriate thromboses (clot formations).

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6
Q

What is another name for platelets?

A

Thrombocytes.

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7
Q

Which X2 layers of the blood vessels are involved in the vascular control of platelets function (activating/mediating them)?

A

The endothelial cells of the tunica intima answer the smooth muscle cells of the tunica media.

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8
Q

What does NO stand for? Where is it released from and what does it do?

A

Nitrous oxide

It is released from the endothelial cells and has a NEGATIVE effect on platelet activation and vasculature smooth muscle cell contraction.

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9
Q

What’s does PGI2 stand for? Where is it released from and what does it do?

A

Prostaglandin I2

Or

Prostacyclin

It is released from the endothelial cells and has a NEGATIVE effect on platelet activation and vasculature smooth muscle cell contraction.

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10
Q

What does EDHF stand for? Where is it released from and what does it do?

A

Endothelium derived hyperpolarising factor.

It is released from the endothelial cells and has a NEGATIVE effect on vasculature smooth muscle cell contraction.

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11
Q

What does ET-1 stand for? Where is it released from and what does it do?

A

Endothelin 1

As it’s name suggests it is released from the endothelial cells and has a POSITIVE effect on vasculature smooth muscle contraction.

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12
Q

What does TXA2 stand for? Where is it released from and what does it do?

A

Thromboxane A2

As it’s name suggests it is released from ACTIVATED platelets (thrombocytes) and has a POSITIVE effect on vasculature smooth muscle contraction. It utilises the cycle-oxygenase 1 (COX-1) enzyme to do this.

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13
Q

What is the difference between primary and secondary haemostasis?

A

Primary = formation of a “platelet plug” at the endothelial wall

Secondary = activation of the clotting cascade and clot stabilisation via fibrin

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14
Q

Describe primary haemostasis.

A

1) blood vessels are damaged
2) platelets are exposed to collagen in the ECM causing them to activate and adhere. This is strengthened by Von Willebrand Factor (vWF) (usually circulating found to FVIII) binding to the collagen.
3) the activated platelets release TXA2 which stimulated vascular vasoconstriction.
4) a soft platelet plug is formed

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15
Q

What are the phases of the clotting cascade?

A

The extrinsic pathway (initiation) and the intrinsic pathway (amplification and propagation) both leading to a final common pathway.

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16
Q

What is another name for the intrinsic pathway of the clotting cascade?

A

Amplification and propagation.

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17
Q

What is another name for the extrinsic pathway of the clotting cascade?

A

Initiation

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18
Q

What activates the initiation pathway and what type of structure is this?

A

Tissue factor (Tf) - a transmembrane receptor.

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19
Q

Where is TF usually found?

A

Cells of the vasculature not usually in contact with flowing blood. It is EXTRINSIC to the system hence the old initiation pathway name.

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20
Q

What does the nomenclature FVIa mean?

A 
F = factor
VI = Roman numeral of the factor (6 in this example)
a = activated
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21
Q

Which clotting factor does TF bind to when vessel damage occurs, and where is this usually found?

A

TF binds to FVII (usually found circulating in the blood) to form a TF:FVIIa complex as FVII is activated…

TF + FVII ——-> TF:FVIIa complex

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22
Q

What does TF:FVIIa active:

(A) in the initiation phase

(B) in the amplification and propagation phase

A

(A) FX ——> FXa

(B) FIX ——> FIXa

23
Q

What is the first activation of the final common pathway?

A

FX ——> FXa

24
Q

What is FII most commonly called?

A

Prothrombin

25
Q

What is FIIa most commonly called?

A

Thrombin.

26
Q

What clotting factor does FXa activate?

A

FXII (prothrombin) ——> FXIIa (Thrombin)

27
Q

What is FI commonly called?

A

Fibrinogen.

28
Q

What is FIa commonly called?

A

Fibrin.

29
Q

What does FIIa activate?

Where does this process occur?

A

FI (fibrinogen) ——> FIa (Fibrin)

On the surface of activated platelets (as FI is bound to them via gp ii beta/iii alpha receptors) forming a fibrin mesh.

30
Q

What does thrombin activate and where does this occur?

A

The cleavage of fibrin from fibrinogen on the surface of activated platelets, to form fibrin strands/mesh stabilising the platelet clot.

31
Q

What process does FXa carry out alone and what can it complex with to optimise this process?

What is this complex called?

A

FXa activates prothrombin (FII) to form thrombin (FIIa)

It is optimised when in a FXa:FVa complex (with the FVa arising in the amplification and propagation (intrinsic) pathway)

The FXa:FVa complex is called PROTHROMBINASE

32
Q

What does thrombin do to platelets?

A

Activates them.

33
Q

In the beginning of the amplification and propagation (extrinsic) pathway, what does the thrombin from the initiation (intrinsic) pathway do?

A

It causes FV to be released and activated from alpha-granules in activated plates, expressing FVa on the platelets surface.

34
Q

What is the second thing thrombin does in the amplification and propagation pathway?

A

It cleaves FVIII from vWF:FVIII complex and activates FVIII to FVIIIa, expressing it on the activated platelets surface.

35
Q

What does FVIIIa on the platelet surface and FIVa complex to form? And what does this do?

A

TENASE -a factor activator.

It also activates FX to FXa (as well as TF:FVIIa complex)

36
Q

Where is fibrinogen usually found and where is it found during platelet activation?

Which receptors does it utilise to bind to this structure?

A

Usually freely circulating in the plasma, but will be found bound to activated platelet surfaces via gp ii beta / iii alpha receptors.

37
Q

Does thrombin stick to fibrin once it has activated it?

A

Yes

38
Q

What factor does thrombin also activate which aids the stabilisation of cross-linked fibrin in a stable clot?

A

FXIII —-> FXIIIa (Factor 13)

39
Q

What is atherosclerosis?

A

A build up of plaque in the arteries.

40
Q

What are the components of an atherosclerotic plaque?

A

A lipid rich core separated from the lumen by a fibrous cap.

41
Q

What is Virchow’s triangle?

Name the X3 components.

A

X3 triangulated factors that describe an increased disposition to thrombosis, they are:

  • stasis of blood
  • endothelial injury
  • hyper-coagulability
42
Q

What is the difference between an arterial and venous thrombi?

A

Arterial

  • “White clots” (despite name) due to a large PLATELET component (as blood in the arterial system is travelling at higher pressures/velocity)
  • Usually associated with atherosclerosis at sites of vessel wall injury

Venous

  • “Red clots” (despite name) due to a large RBC component (as blood in the venous system is travelling at lower pressures/velocity so is likely to pool)
  • Usually due to stasis of blood
43
Q

What are the X3 types of drugs used to combat thrombosis?

A

Antiplatelets

Anticoagulants

Fibrinolytics (clot busters)

44
Q

What type of thrombosis are antiplatelet drugs most likely to be used for?

A

Arterial thrombosis (white clots) due to their high platelet content.

45
Q

Name X3 types of antiplatelet drugs/mechanisms?

A

Asprin

P2Y12 antagonists

GP ii beta/iii alpha antagonists

46
Q

How does Asprin work?

A

It is a irreversible inhibitor of the cyclo-oxygenase 1 (COX-1) enzyme found in platelets. COX activation in platelets causes them to produce TXA2 (thromboxane A2) which is a platelet agonist and vasoconstrictor (as seen before). Inhibiting this therefore inhibits platelet activation/aggregation.

47
Q

What are prostaglandins and what are they synthesised from?

Which enzyme/s are involved in this process?

Which group of drugs limit the production of prostaglandins via inhibition of these enzymes?

A

They are cell signalling molecules involved in the inflammatory and pain responses.

They are synthesised from arachindoic acid via the COX-1 & 2 enzymes.

NSAIDS inhibit the COX enzymes.

48
Q

How does Asprin affect thromboxane and not PGI2?

A

The endothelium can continually and quickly synthesise the COX-2 enzyme and therefore PGI2, meaning it is still present to work as a platelet antagonist and vasodilator.

49
Q

Name some P2Y12 receptor antagonists?

A

ALL HAVE ‘GREL’ in them somewhere!!!

Have an active metabolite stage:

  • Clopidogrel
  • Prasugrel

Have no active metabolite stage:

  • Ticagrelor
  • Cangrelor
  • Elinogrel
50
Q

Where are P2Y12 receptors found and what do they do?

A

They are found on platelets and cause amplification and aggregation of platelets by binding with ADP to activate the GP ii beta/iii alpha receptor complex. Antagonists of P2Y12 therefore inhibit this process.

51
Q

Name X2 classes of GP ii beta/iii alpha antagonists with examples for each.

A

Small antibody (fab) fragments

  • Abciximab
  • Tirofiban

Small molecule inhibitors
- Eptifibatide

52
Q

How do GP ii beta/iii alpha antagonists work?

A

They compete with fibrinogen for the receptor. It is the multiple binding of fibrinogen to these platelet receptors which causes them to aggregate, therefore by inhibiting this process the aggregation of platelets can not occur, making this class effective as anti-platelet drugs.

53
Q

What is thrombocytopenia and which anti-platelet class of drugs carries a risk of this if used long term?

A

Low blood platelet count

GP ii beta/iii alpha antagonists

Physiology & Pharmacology of Systems (21 decks)

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