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Haematology and Immunology > Haemostasis - Bleeding and Thrombosis > Flashcards

Haemostasis - Bleeding and Thrombosis Flashcards

1
Q

What is the key job of the endothelium lining the blood vessel wall?

A

To prevent cells from sticking to the surface and therefore encourages flow

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2
Q

What lines an intact blood vessel wall?

A

Endothelium

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3
Q

What does endothelium produce to make it non-stick?

A

Heparins
Anticoagulants e.g. TFPI, thrombomodulin
Prostacyclin
Nitric oxide

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4
Q

What does prostacyclin prevent?

A

White cells and platelets from sticking to vessel walls

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5
Q

What do you need to form a clot?

A

Platelets
vWF - a big sticky factor
Coagulation factors

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6
Q

What do coagulation factors do?

A

They become activated in a coagulation cascade to produce a fibrin clot

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7
Q

What do natural anticoagulants do?

A

Once an adequate clot is formed, these substances switch off the clot
So they tell the clot that it has done its job and to stop.
Therefore the clot stops forming and is remained confined to the site of the injury

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8
Q

What removes the clot once it has done its job?

A

The fibrinolytic system

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9
Q

How is a clot localised?

A

Signals
Abnormal surface
Localised physiological activator

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10
Q

What happens when there is vessel damage?

A

Platelet adhesion
- platelets see the subendothelial collagen and stick to it - becoming sticky and active
Von Willebrand factor also has binding sites for collagen and platelets so it sticks to these to start to make the clot
Physiological activators are very localised

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11
Q

Platelets have a series of receptors

A

ADP receptors
Epinephrine receptors
Thrombin receptors
Glycoprotein receptors

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12
Q

What is inside a platelet?

A

Granules containing important chemicals involved in coagulation

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13
Q

Glycoprotein receptors of platelets and what they bind to

A

GP ia/iia binds to collagen in a damaged wall
GP iib/iiia binds to fibrinogen
GP Ib binds to von Willebrand factor

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14
Q

Platelets function in homeostasis

A

Adhere
- glycoproteins binding to factors
- holding the platelet in place where there is tissue damage
Activation
- ADP pathway (P2Y12)
- Cyclooxygenase pathway producing thromboxane
Aggregation (stick)
- thromboxane allows platelets to stick
- phospholipid membrane produced by scramblase enzyme
Provides phospholipid surface for coagulation proteins to be activated upon

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15
Q

Features of von Willebrand factor

A

Big protein around areas of damage
Contains binding sites
Capable of sticking to all the things you want it to - things that are exposed during tissue damage
Also can bring factor VIII into area of tissue damage

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16
Q

What is a primary haemostatic (platelet) plug?

A

After damaged blood vessel, platelets adhere and become activated, and bind fibrinogen
This plug on its own is not enough - it is weak and will fall apart unless stabilised by a fibrin clot

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17
Q

What is definitive haemostasis?

A

Fibrin formation

Formation of fibrin clot on top of the platelet clot

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18
Q

Clotting agents (cascade effect)

A 
Factor XII
Factor XI
Factor IX
Factor VIII
Factor X 
Prothrombin 
Fibrinogen
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19
Q

Normal clotting sequence

A

Fibrin net and platelets plugs at hole in vessel wall in an injury or surgery
Fibrin clot = prevents bleeding from area of damage

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20
Q

What do anticoagulants to?

A

Resist and stop clotting factors, affecting the whole process/cascade

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21
Q

What would happen in the clotting if a factor was missing?

A

The process would become not complete, the fibrin clot does not form and the blood continues to come from the damaged vessel

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22
Q

In haemophilia A, what factor is deficient?

A

Factor VIII

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23
Q

In haemophilia B, what factor is deficient?

A

Factor IX

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24
Q

What binds with factor VII to activate it?

A

Tissue factor

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25
Q

What does the conversion of prothrombin to thrombin lead to?

A

The conversion of fibrinogen to fibrin

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26
Q

What happens to fibrinogen ontop of platelets?

A

It is cleaved to form a fibrin clot

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27
Q

Types of natural anticoagulants

A

TFPI (tissue factor pathway inhibitor)

  • binds to and inactivates forms of coagulation factors
  • when switches off one or two - then reduces the amount of fibrin which stops the clot forming

Protein C and S

  • switching off clotting factors
  • reducing the amount of thrombin and therefore reducing the clot

Antithrombin
- Inactivates factor 10 and THROMBIN

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28
Q

Most important natural anticoagulant

A

Antithrombin

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29
Q

What is fibrinolysis?

A

Breaking down the clot - the first stage to tissue repair

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30
Q

What happens in fibrinolysis?

A

Once the clot is formed, this becomes the dominant feature
Endothelium produces activators of plasminogen
- t-PA main one
- u-PA
Plasminogen is cleaved by t-PA to produce active plasmin which breaks down the fibrin clot to reorganise the vessel

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31
Q

Regulation of fibrinolysis

A 
Inhibitors
- PA1-1
- PA2-2
Inhibitors of plasmin (not that significant)
- A2 - antiplasmin 
- A2 - macroglobulin
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32
Q

What is a D dimer?

A

A bit of fibrin broken down by plasmin

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33
Q

Antithrombotic/anticoagulant drugs

A

Warfarin
Heparins
Dalbigatran

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34
Q

Antiplatelet drugs

A

Aspirin
Clopidogrel/prasugrel/ticagrelor
Tirofiban/eptifibatide/abciximab

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35
Q

What does aspirin do?

A

Prevents platelets from being sticky

It can inhibit thromboxane - less likely to form clots in vessels

36
Q

What does tirofiban/epitifibatide/abciximab do?

A

prevents activated glycoproteins from binding to fibrinogen

37
Q

What does warfarin do?

A

Reduces the amount of 4 of the coagulation factors

  • 2, 7, 9 and 10
  • Vitamin K dependents
  • prevents these levels by inhibiting vitamin K
  • can reverse it by giving them vitamin K e.g. in bleeding
38
Q

How do dabigatran etc work?

A

Oral inhibitor of thrombin

39
Q

How do DOACs (direct oral anticoagulants) work?

A

Bind to active site of factor Xa and stop it from working

40
Q

Two ways to initiate a clot

A
  1. Damaged surface - intrinsic pathway

2. Tissue factor - extrinsic pathway

41
Q

What does thrombin convert?

A

Fibrinogen to fibrin

42
Q

What is haemophilia?

A

The tendency to bleed

43
Q

Why is cancer a hypercoagulable state?

A

Inflammatory cytokines
Less mobile
Chemo

44
Q

Hypercoagulable states

A 
Nephrotic syndrome
Malignancy 
OCP / oestrogen therapy
Pregnancy 
Trauma
IBD
Sepsis
Thrombophilia
45
Q

What causes circulatory stasis?

A 
AF
LV systolic dysfunction 
Immobility
Venous insufficiency e.g. varicose veins
Venous obstruction e.g. pelvic tumour, obesity, pregnancy
46
Q

Symptoms of PE

A

Pleurisy
Chest pain
SOB

47
Q

What does Wells score tell us?

A

The probability of PE / DVT

48
Q

What scores of the wells score are PE unlikely and likely?

A

Likely > 4

Unlikely < 4

49
Q

What scores of the wells score are DVT unlikely and likely?

A

Likely > 2

Unlikely < 1

50
Q

What is used to investigate a DVT?

A

D-dimer

Doppler

51
Q

When is a doppler used to investigate a suspected DVT?

A

If wells score > 2

52
Q

What is rivoroxaban?

A

An anticoagulant

53
Q

What does rivoroxaban block?

A

Factor Xa

54
Q

What does heparin promote?

A

Antithrombin

55
Q

How does warfarin work?

A

Affects protein C and S first

Blocks vitamin K (need this to make factors active)

56
Q

What is used with warfarin? When?

A

LMWH

Not active before INR becomes therapeutic

57
Q

What do protein C and S do?

A

Accelerate destruction of VIII and V

58
Q

When is there a high rate of relapse of DVT / PE? Therefore how long would you carry on treatment for?

A

First 3 - 6 months

Carry on Tx for 6 months

59
Q

What involves thromboprophylaxis?

A

LMWH
Stockings
Mobilisation

60
Q

Causes of thrombophilia

A 
Acquired (5 most common)
- malignancy 
- nephrotic syndrome
- antiphospholipid syndrome
- heparin induced thrombocytopenia 
Hereditary 
- protein C or S deficiency 
- Prothrombin mutation 
- Factor V leidein mutation 
- Antithrombin III deficiency
61
Q

What type of inheritance is factor V Leiden deficiency?

A

Autosomal dominant

62
Q

How does factor V leiden work?

A

Resists destruction from protein C

63
Q

What factors does protein C destroy?

A

5 and 8

64
Q

What type of inheritance is Protein C and S deficiency?

A

Autosomal dominant

65
Q

What type of inheritance is antithrombin III deficiency?

A

Autosomal dominanttt

66
Q

Acquired causes of antithrombin III deficiency

A

nephrotic syndrome
Liver disease
DIC
pregnancy

67
Q

Does liver disease make you bleed or clot?

A

Both

Due to not making either of the factors

68
Q

Diagnosis of thrombophilia

A

Test for genes
Test for factors
Check for antiphospholipid syndrome

69
Q

What can be the first sign of cancer in some people?

A

Clot

70
Q

Who gets purpura fulminans?

A

Children

71
Q

Why is thrombophilia testing in pregnancy less reliable?

A

As you are already protein S deficient

72
Q

Pathology of heparin induced thrombocytopenia

A

Antibodies against heparin as body sees it as foreign

73
Q

How long after heparin does HIT take to develop?

A

5 - 10 days after as antibodies take time to make

74
Q

Tx of HIT

A

Take off

Give alternative

75
Q

What stops you bleeding?

A

Vascular constriction
Collagen and von Willebrand factor exposed
Platelet activation, adherence and aggregation
Platelet plug formed

76
Q

How many platelets are needed for surgery?

A

100

77
Q

How many platelets are needed for minor surgery?

A

50

78
Q

What level of platelets do purpura appear?

A

< 30

79
Q

What level of platelets do spontaneous bleeding occur?

A

< 10

80
Q

Causes of thrombocytopenia

A

Liver disease - reduced thrombopoietin production
Bone marrow failure
Platelets pooled in enlargened spleen
Major haemorrhage
DIC
Autoimmune platelet destruction (immune thrombocytopenic purpura)
HIT

81
Q

Causes of reduced marrow production

A

Cancer
Chemo
Aplastic anaemia
Vitamin deficiency (B12 or folate)

82
Q

Who does ITP occur in?

A

Children and teenagers often after a viral illness e.g. glandular fever
Autoimmune in adults

83
Q

When should ITP be treated?

A

If platelets < 30

84
Q

Pathology of DIC

A

Tissue factor can be activated by endotoxin, snake bites, TNF etvc
Activated factor VII, and also IX, XI, and XII
Excess thrombin binds to fibrinogen, thus creating fibrin clots which trap platlets
This causes clot using up platelets and clotting factors

85
Q

Tx of DIC

A

Remove underlying cause
FFP
Platelets

86
Q

Tx of ITP

A

Steriods / immunosuppressants
IV immunoglobulins
Spleenectomy
Dapsone / anti D

87
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

Haematology and Immunology (18 decks)

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