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POM > Haem - Haemostasis > Flashcards

Haem - Haemostasis Flashcards

1
Q

What is haemostasis?

A

Blood clot

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2
Q

Steps in haemostasis

A
  1. Vasoconstriction
  2. Primary haemostasis
  3. Secondary haemostasis
  4. Fibrinolysis
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3
Q

What is primary haemostasis?

A

Formation of unstable platelet plug (Platelet adhesion/aggregation)

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4
Q

What is secondary haemostasis?

A

Formation of stable fibrin clot

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5
Q

What is fibrinolysis?

A

Dissolution of a clot

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6
Q

Important balances in haemostasis

A
  1. Coagulation (state change)
  2. Thrombosis (Limit area)
  3. Fibrinolysis (breakdown clot, healing)
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7
Q

Where are platelets formed?

A

In the bone marrow, derived from myeloid stem cells, it is a fragmentation of megakaryocyte cytoplasm

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8
Q

What is von Willebrand factor VWF?

A

Factor in mediating platelet adhesion, also promotes platelet-platelet aggregation

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9
Q

What happens in primary haemostasis?

A
  1. Platelet stick to damaged endothelium (…)
  2. Adhesion activates platelets (…)
  3. Platelet aggregates
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10
Q

How does platelet stick to endothelium?

A

Either directly to collagen via GP1a receptor
OR
indirectly to the VWF factor with binds to GP1b receptor

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11
Q

How does adhesion activate platelet?

A
  1. Membrane invaginated to release content of granules
    - ADP, fibrinogen, VWF
  2. Changes shape (round w/ spicules) - increase platelet-platelet interaction
  3. Produces prostaglandin thromboxane A2
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12
Q

What are the granules of platelet?

A
  • alpha-granule

- dense granule

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13
Q

What does thromboxane A2 do?

A
  1. Promotes platelet aggregation

2. Vasoconstrictor (imp. in injury & inflammation)

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14
Q

What signals further activation and aggregation in primary haemostasis?

A

Combo of ADP & thromboxane, giving positive feedback

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15
Q

How does platelet further aggregate?

A

By binding to ADP (P2Y12) and thromboxane A2 receptors

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16
Q

How does ADP + ThA2 cause further activation?

A

Conformational change in GPIIb/IIIa receptor, provide binding site - fibrinogen- to link platelet to form plug

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17
Q

What chemical counter balances and stops platelet aggregation?

A

Prostacyclin (GPI 2) - powerful vasodilator & suppress platelet adhesion

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18
Q

What is secondary haemostasis?

A

Clotting involving the coagulation cascade

[formation of fibrin]

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19
Q

What HAPPENS in secondary haemostasis?

A

Generation of thrombin –> cleaves fibrinogen –> form fibrin clot –> stabilise plug

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20
Q

What is factor II?

A

Prothrombin

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21
Q

What does the synthesis of clotting factors depend on?

A 
Vitamin K (for carboxylation of glutamic acid residue)
essential for clot function
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22
Q

What do clotting factors work on?

A

Exposed platelet phospholipid surfaces (help localise & accelerate reactions)

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23
Q

Where are clotting factors synthesised?

A

Liver (except for factor VIII & VWF - endothelial cell)

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24
Q

What initiates coagulation?

A

Tissue factor - not normally exposed to blood, only injury

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25
Q

How does tissue factor initiate coagulation?

A

It binds to factor VIIa
- activates factor IX –> XIa
- activates factor X –> Xa
Activates prothrombin (Factor II)

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26
Q

What are the 3 phases of secondary haemostasis?

A
  1. Initiation
  2. Amplification
  3. Propagation
27
Q

What does activating prothrombin do?

A

Generate thrombin (factor IIa)

28
Q

What does thrombin do? (propagation)

A

Cleaves soluble fibrinogen to insoluble fibrin

29
Q

What does small amount of thrombin mediate?

A

Activation of cofactor V & VIII, zymogen (factor XI) & platelets

30
Q

What is the amplication phase?

A

Zymogen converts more FIX –> FIXa
FIIIA converts more FX –> FXa
Therefore, more thrombin (FIIa) converted from Prothrombin (FII)

31
Q

What ion is important in binding activated clotting factors to phospholipid surfaces?

A

Calcium ion

32
Q

What does Zymogen (FXI) turn?

A

Activate clotting co-factors
FV –> FXI
FVIII –> FVIIIa
(by splitting of peptide bonds & expose enzyme sites)

33
Q

What happens during fibrinolysis?

A

Tissue plasminogen activator (t-Pa) activates plasmin by binding to lysine residue on fibrin

Fibrin is broken down into Fibrin-degradation products (FDPs)

34
Q

What was plasmin before it was activated?

A

Inactive Plasminogen

35
Q

What do anti-platelet drugs do?

A

Prevention and treatment of cardiovascular/cerebrovascular disease

36
Q

How does anti-platelet drugs work?

A
  • Inhibit thromboxane A2 production
  • Block ADP receptor

Hence decrease platelet aggregation, and prevent formation of thrombus

37
Q

What are some examples of anti-platelet drugs?

A

Aspirin, Clopidogrel

38
Q

How long does anti-platelet drug last?

A

Until new platelets are produced (around 7 days)

39
Q

What do thrombolytic therapy/agents do?

A

eg Recombinant t-Pa intravenously injected to generate plasmin to breakdown clots

40
Q

What is the risk w/ thrombolytic therapy?

A

Bleeding

41
Q

What are thrombolytic therapies used for? What replaced them?

A

Ischaemic stroke
Myocardial infarction
Life-threatening pulmonary emboli
(Stents, angioplasty)

42
Q

How does antifibrinolytic drug (Tranexamic acid) work?

A

Competitive inhibition - derivative of lysine

  1. binds to plasminogen
  2. prevent bind to lysine residue of fibrin
  3. prevent activation of plasmin
43
Q

What are antifibrinolytic drugs used for?

A

Treat bleeding in:

  • Trauma surgical patients
  • Inherited bleeding disorders
44
Q

What happens when the balance leans towards fibrinolytic factors and anticoagulant proteins?

A

Bleeding

  • reduce platelet function
  • reduce coagulator factors
  • increase fibrinolysis
45
Q

What happens when the balance leans towards coagulation factors and platelets?

A

Thrombosis - clot in vessel

  • reduce anticoagulant proteins
  • reduce fibrinolysis
  • increase clotting factor/platelet
46
Q

Coagulation inhibitory mechanism:

A
  1. Thrombin binds thrombomodulin
    - activates Protein C –> “activated protein C (APC)”
  2. APC activates FVa &FVIIIa in presence of cofactor Protein S
  3. Thrombin & FXa inactivated by Antithrombin
47
Q

How does heparin increase action of antithrombin?

A

Antithrombin binding to endothelial cell-associated heparin

48
Q

What use is the anticoagulant pathway?

A

To confine coagulation at site of injury

49
Q

What are the main substrates for anticoagulation?

A

Protein C
Protein S
Antithrombin

50
Q

What are some examples of anticoagulant drugs? (prevent thrombosis)

A

Heparin, Warfarin, Direct Oral Anticoagulants (DOACs)

51
Q

How does Heparin drug work?

A

Potentiate action of antithrombin –> inactivate FXa and thrombin

52
Q

How does Warfarin drug work and monitored?

A

Oral tablet

  • Interferes protein carboxylation / antagonizes Vitamin K
  • Reduces synthesis of vit K-dependent clotting factors (thrombin, VII, IX, X) produced by liver

Monitored by regular blood tests

53
Q

How does Direct oral anticoagulants drug work and monitored?

A

Directly inhibits either thrombin/FXa

No monitor

54
Q

What are the tests of coagulation?

A
  • PT (Prothrombin time)

- APTT (Activated partial thromboplastin time)

55
Q

What does prothrombin time measure?

A

Time to clot following extrinsic pathway

56
Q

What does aPTT measure?

A

Time to clot following intrinsic pathway

57
Q

How to do a PT test?

A
  1. Blood collected in bottle w/ sodium citrate (chelates Calcium to initially prevent clot)
  2. Sample spun - produce platelet-poor plasma
  3. Add Tissue factor & phospholipid + calcium

Time…

58
Q

What does a ‘prolonged PT’ tell you?

A

Reduction in activity of FVII, X, II prothrombin, fibrinogen

59
Q

How to do an aPTT test?

A

Add contact activator, phospholipid, citrated plasma and calcium

Time…

60
Q

What does a ‘prolonged aPTT’ tell you?

A

Reduced in one/more clotting factor

61
Q

What does a ‘prolonged aPTT’ and ‘normal PT’ tell you?

A

Haemophilia A (FVIII deficient)

Haemophilia B (FIX deficient)

Haemophilia C (FXI deficient)

FXII deficient (does not result in bleeding, wrong in model)

62
Q

What is the combination name of Tissue factor and phospholipid?

A

Recombinant thromboplastin

63
Q

What does INR stand for?

A

International normalized ratio

POM (22 decks)

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