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BRS YR2 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is Haemostasis?

A

the cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult

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2
Q

What is the aim of haemostasis?

A
  • prevention of blood loss from intact vessels
  • arrest bleeding from injured vessels
  • enable tissue repair
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3
Q

What are the four stages of Haemostasis?

A
  • vessel constriction
  • formation of an unstable platelet plug (primary haemostasis)
  • stabilisation of the plug with fibrin (secondary haemostasis)
  • vessel repair and dissolution of clot
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4
Q

What happens when vessel constriction occurs?

A
  • vascular smooth muscle cells contract locally
  • limits blood flow to injured vessel
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5
Q

What happens during primary haemostasis?

A

formation of an unstable platelet plug

  • platelet adhesion
  • platelet aggregation
  • limits blood loss and provides surface for coagulation
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6
Q

What happens during secondary haemostasis?

A

stabilisation of the plug with fibrin

  • blood coagulation
  • stops blood loss
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7
Q

What happens during fibrinolysis?

A

vessel repair and dissolution of the clot

  • cell migration/proliferation and fibrinolysis
  • restores vessel integrity
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8
Q

Why is understanding of haemostatic mechanisms important?

A
  • diagnose and treat bleeding disorders
  • control bleeding
  • identify thrombosis risk factors
  • treat thrombotic disorders
  • monitor drugs used to treat bleeding/thrombotic disorders
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9
Q

What is balanced in normal haemostasis?

A
  • fibrinolytic factors and anticoagulant proteins
    AND
  • coagulant factors
  • platelets
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10
Q

What can cause the lack of a specific factor?

A
  • failure of production (congenital and acquired)
  • increased consumption and clearance
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11
Q

What can cause defective function of a specific factor?

A
  • genetic
  • drugs and other chemicals
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12
Q

What are the 3 main components of primary haemostasis?

A
  • platelets
  • Von Willebrand factor
  • Vessel wall
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13
Q

What do platelets adhere to in direct platelet adhesion?

A

Collagen revealed in wall damage via the GPIa receptor

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14
Q

What do platelets adhere to in indirect platelet adhesion?

A

Collagen revealed in wall damage via VWF which binds to GPIb receptor

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15
Q

What is involved in platelet aggregation?

A
  • adhesion
  • ADP and thromboxane A2
  • platelet activation
  • formation of platelet plug
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16
Q

What happens in adhesion?

A

ADP, fibrinogen and VWF released from storage granules in platelets

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17
Q

What activates platelets in a positive feedback mechanism?

A

ADP and thromboxane A2

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18
Q

What happens when platelets are activated?

A
  • binding sites change from GPIa/GPIb to GPIIa/GPIIb
  • binding sites can now bind fibrinogen
  • fibrionogen links platelets together to form an unstable platelet plug
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19
Q

What does Thrombocytopenia mean?

A

platelet insufficiency

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20
Q

What are the 3 causes of Thrombocytopenia?

A
  • decreased production caused by bone marrow failure
  • Accelerated clearance
  • Pooling and destruction in an enlarged spleen
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21
Q

What can cause bone marrow failure?

A
  • leukaemia
  • B12 deficiency
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22
Q

What causes accelerated platelet clearance?

A
  • immune thrombocytopenia purpura (ITP)
  • Disseminated Intravascular Coagulation (DIC)
    (cleared in the peripheral system)
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23
Q

What happens in Immune Thrombocytopenic Purpura (ITP)?

A
  • anti-platlet antibodies
  • attach to sensitised platlets
  • cleared by macrophages of the reticula endothelial system of the spleen
    (COMMON)
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24
Q

What causes the impaired function of platelets?

A
  • Hereditary absence of glycoproteins or storage granules (rare)
  • Acquired due to drugs
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25
Q

What causes storage pool disease?

A

Reduction in the granular contents of platlets

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26
Q

What drugs are associated with causing impaired platelet function?

A
  • aspirin
  • NSAIDs
  • clopidogrel (common)
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27
Q

When are anti-platelet drugs used?

A

in the prevention and treatment of cardiovascular and cerebrovascular disease

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28
Q

How does aspirin have an anti-platelet effect?

A

aspirin prevents the production of Thromboxane A2 by irreversibly blocking COX enzyme causing reduced platelet aggregation

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29
Q

How does aspirin have an anticoagulant effect?

A

irreversibly blocks the ADP receptor on platelets (P2Y12), preventing platelet activation

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30
Q

What can cause Von Willebrand disease?

A
  • Hereditary: decrease of quantity +/ function (COMMON)
  • Acquired: antibody (rare)
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31
Q

What are the roles of Von Willebrand factor in Haemostasis?

A
  • binding to collagen and capturing platelets
  • stabilising factor VIII
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32
Q

What is the relationship between Von Willebrand Factor and Factor VIII?

A

VWF is needed for Factor VIII, so if VWF is low, so is Factor VIII

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33
Q

What are the 3 different types of Von Willebrand factor problems?

A
  • Type 1/3: deficiency of VWF
  • Type 2: VWF with abnormal function
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34
Q

What can cause inherited problems with the vessel wall?

A

RARE
- Haemorrhagic telangiectasia
- Ehlers-Danlos syndrome
(other connective tissue disorders)

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35
Q

What can cause acquired problems with the vessel wall?

A

COMMON

  • steroid therapy
  • Ageing (senile purpura)
  • Vasculitis
  • Scurvy
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36
Q

What causes VWF to unfold/uncoil?

A

shear force

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37
Q

What does VWD impact in haemostasis?

A

primary haemostasis

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38
Q

What are the clinical features of primary haemostasis disorders?

A
  • immediate bleeding
  • prolonged bleeding from cuts/trauma/surgery
  • nose bleeds (epistaxis) >20mins
  • prolonged gum bleeding
  • heavy menstrual bleeding (menorrhagia)
  • bruising (ecchymosis), spontaneous/easy
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39
Q

What are the visible signs seen in primary haemostasis disorders?

A

Petechiae and Purpura

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40
Q

What is the difference between petechiae and purpura?

A
  • petechiae are smaller (< 3mm)
  • purpura are larger (3-10mm) and do not blanch under pressure
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41
Q

What is a key clinic feature of severe VWD?

A

haemophilia-like bleeding (due to low FVIII)

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42
Q

What are tests are done for primary haemostasis disorders?

A
  • platelet count/morphology (electron)
  • FBC
  • bleeding time (PFA100)
  • VWF assays
  • clinical observation
  • coagulation screen (PT, APTT)
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43
Q

What should be the expected results from the coagulation screen?

A

normal (PT, APTT)
UNLESS
severe VWD cases where factor VIII

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44
Q

How would you treat the failure of production/function in haemostasis disorders?

A

replace missing factor/platelets
- prophylactic
- therapeutic
STOP drugs (aspirin, NSAIDs)

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45
Q

How would you treat the immune destruction in primary haemostasis disorders?

A
  • immunosuppression via corticosteroids (prednisolone)
  • splenectomy for ITP as second line
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46
Q

How would you treat the increased consumption/clearance in haemostasis disorders?

A
  • treat cause
  • replace as necessary
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47
Q

What additional treatments can be used to support haemostasis?

A
  • Desmopressin
  • Tranexamic acid (antifibrinolytic)
  • Fibrin glue/spray post surgery
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48
Q

What is Desmopressin?

A

Vasopressin analogue

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49
Q

What does Desmopressin do?

A
  • 2-5 fold increase in VWF (+ Factor VIII)
  • releases endogenous stores (only used in mild disorders)
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50
Q

What is another name for secondary haemostasis?

A

coagulation

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51
Q

What is the role of coagulation?

A
  • generate thrombin (Factor IIa) - which converts fibrinogen to fibrin
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52
Q

What is the result of a coagulation factor deficiency?

A

failure of thrombin generation and therefore fibrin formation

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53
Q

What are the 3 phases of coagulation?

A
  • initiation
  • amplification
  • propagation
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54
Q

Which factors are part of the extrinsic pathway?

A
  • Tissue factor (factor VIII)
  • Factor VII (binds to TF)
  • Factor IX and factor
55
Q

Which factors are part of the intrinsic pathway?

A
  • Thrombin (factor II)
  • Factor XI
  • Factor VIII
56
Q

What can cause disorders of coagulation?

A
  • deficiency of coagulation factor production
  • dilution
  • increased consumption
57
Q

What hereditary causes are there for the deficiency of coagulation factor production?

A
  • haemophillia A (facotr VIII deficiency)
  • haemophillia B (factor IX deficiency)
58
Q

What acquired causes are there for the deficiency of coagulation factor production?

A
  • liver disease
  • anticoagulant drugs
    (warfarin, DOACs)
59
Q

What are the acquired causes of dilution?

A

blood transfusion (with inadequate plasma replacement)

60
Q

What are the acquired causes of increased consumption/clearance?

A

COMMON: Disseminated intravascular coagulation (DIC)
RARE: immune (autoantibodies)

61
Q

What are the 2 common hereditary coagulation disorders?

A

Haemophilia A (FVIII) + B (FIX)

62
Q

What happens in haemophilia?

A

failure to generate fibrin to stabilise the platelet plug

63
Q

What is the hallmark of haemophilia?

A

haemarthrosis

64
Q

What is Haemarthrosis?

A

spontanteous joint bleeding (very low FVIII and FIX)

65
Q

What happens in chronic haemarthrosis?

A
  • recurrent spontaneous bleeds
  • significant joint deformity
  • muscle wasting
66
Q

What should be avoided in patients with haemophilia?

A

avoid IM injections

67
Q

What is the impact of the absence of Factor VII and Factor IX?

A
  • severe but compatible with life
  • spontaneous joint and muscle bleeding
68
Q

What is the impact of the absence of Factor II (Prothrombin)?

A

Lethal

69
Q

What is the impact of the absence of Factor XI?

A

bleed after trauma, but not spontaneously

70
Q

What is the impact of the absence of Factor XII?

A

no bleeding at all

71
Q

What is the impact of liver failure on coagulation?

A

decreased, as most clotting factors are synthesised in the liver.

72
Q

What is the impact of dilution on coagulation?

A
  • red cell transfusions don’t consider plasma
  • major haemorrhage requires transfusion of plasma as well as RC and platelets to prevent.
73
Q

What is Disseminated intravascular coagulation?

A

generalised (and unregulated) activation of coagulation - Tissue factor

74
Q

What can trigger Disseminated Intravascular Coagulation?

A
  • sepsis
  • major tissue damage (cancer)
  • inflammation
75
Q

Wjhat happens in Disseminated Intravascular Coagulation?

A
  • consumption and depletion of coagulation factors
  • consumed platelets (thrombocytopenia)
  • activation of fibrinolysis depletes fibrinogen (raised D-dimer)
  • fibrin deposit in vessels can cause organ failure
76
Q

Why is D-dimer raised in Disseminated Intravascular Coagulation?

A

D-dimer is a product of fibrin breakdown

77
Q

How do you manage Disseminated Intravascular Coagulation?

A

Replacemnet of missing coagulation factors

78
Q

What characterises Disseminated Intravascular Coagulation?

A

combined clotting and bleeding pattern

79
Q

What are the clinical features of coagulation disorders?

A
  • superficial cuts do not bleed
  • common: bruising, rare: nosebleeds
  • spontaneous bleeding is deep (muscles or joints)
  • bleeding after trauma is delayed/prolonged
  • bleeding may restart after stopping
80
Q

Why do superficial cuts not bleed?

A

small, therefore platelets can form a plug

81
Q

How can you clinically distinguish between platelet and coagulation defects?

A
  • where the bleeding occurs
  • time for bleeding after trauma/injury
82
Q

What is the difference in bleeding in platelet and coagulation defects?

A

Platelet:
- superficial bleeding into skin and mucosal membranes
Coagulation:
- bleeding into deep tissues, muscles and joints

83
Q

What is the difference in time for bleeding after injury in platelet and coagulation defects?

A 
Platelet:
- bleeding immediate after surgery
Coagulation
- delayed, but severe after injury
- often prolonged
84
Q

What tests are available for coagulation disorders?

A 
Screening
- Prothrombin time (PT)
- Activated partial thromboplastin time (APTT)
- FBC (platelets)
Coagulation factor assays
Tests for inhibitors
85
Q

What does prothrombin time measure?

A

the extrinsic pathway

86
Q

What does the Activated Partial Thromboplastin Time (APTT) measure?

A

the intrinsic pathway

87
Q

What do we use to trigger the Prothrombin Time (PT)?

A

Tissue factor (recombinant)

88
Q

What do we use to trigger the Activated Partial Thromboplastin Time (PT)?

A

by contact activation with NO

89
Q

What would cause a normal PT time but an prolonged APTT?

A
  • haemophilia A/B
  • Factor XI deficiency
  • Factor XII deficiency
90
Q

Why is APTT elongated in haemophilia A/B?

A

many of the factors in the intrinsic pathway are affected by a deficiency

91
Q

What would cause a prolonged PT time but a normal Activated Partial Thromboplastin time?

A
  • Factor VII deficiency
92
Q

What would cause a prolonged PT time and a prolonged APTT?

A
  • Liver disease
  • anti-coagulant drugs
  • DIC
  • Dilution
    (deficiency of the factors of the common pathway)
93
Q

What factors are part of the common pathway?

A
  • FX
  • FV
  • FII
94
Q

What are the principles of abnormal secondary haemostasis?

A
  • failure of production
  • immune destruction
  • increased consumption
95
Q

What are the 4 different types of factor replacement therapy?

A
  • Plasma (Fresh Forzen Plasma)
  • Cryoprecipitate
  • Factor concentrates
  • Recombinant forms of FVIII and FIX
96
Q

What is in Fresh Frozen Plasma (FFP) and what is it used for?

A
  • contains all coagulation factors
  • DIC
97
Q

What is in cryoprecipitate and what is it used for?

A
  • rich in: fibrinogen, FVIII, VWF and FXIII
  • hypofibrinogenemia, VWD, haemophillia A
98
Q

What is in factor concentrates and what are they used for?

A
  • available for all factors apart from FV
  • specific factor deficiencies
99
Q

What are recombinant forms of FVIII and FIX used for?

A

Haemophillia A and B

100
Q

What are the future possible treatments of haemophilia?

A
  • prolonged half life
  • gene therapy
  • novel agents
101
Q

What are the risks of haemophilia treatment?

A
  • safety
  • potential of transfer of blood borne pathogens
102
Q

What are the novel treatments available?

A
  • gene therapy (haemophilia A/B)
  • bispecific antibodies (haemophilia A)
  • RNA silencing (haemophilia A and B)
103
Q

What additional haemostatic treatments are available for anti-coagulant blood disorders?

A
  • desmopressin
  • tranexamic acid
  • fibrin glue/spray
  • other indirect (treat symptoms, like: OCP)
104
Q

What can cause an increase in fibrinolytic factors and anti-coagulant proteins?

A

induced by drugs:

  • tPA - tissue plasminogen activator (stroke)
  • Heparin
105
Q

What is thrombosis?

A
  • intravascular coagulation
  • inappropriate coagulation
  • venous or arterial
  • obstructs flow
  • may embolise to the lungs
106
Q

What is Virchow’s triad?

A

the 3 factors that contribute to thrombosis

107
Q

What is in Virchow’s triad?

A
  • reduced blood flow
  • vascular injury
  • hypercoagulability
108
Q

What is the impact on risk when there are changes in blood hypercoagulability in Virchow’s triad?

A

dominant in venous thrombosis

109
Q

What is the impact on risk when there is vascular injury in Virchow’s triad?

A

dominant in arterial thrombosis

110
Q

What is the impact on risk when there is decreased blood flow in Virchow’s triad?

A

contributes to both arterial and venous thrombosis

111
Q

What are the presentations of a pulmonary embolism?

A
  • tachycardia
  • hypoxia
  • shortness of breath
  • chest pain
  • haemoptysis
  • sudden death
112
Q

What is the presentation of deep vein thrombosis?

A
  • painful leg
  • oedema
  • erythema
  • warm
  • embolise to lung
  • post thrombotic syndrome
113
Q

What is thrombophilia?

A

increased risk of venous thrombosis

114
Q

How does thrombophilia present?

A
  • thrombosis at a young age
  • spontaneous thrombosis
  • multiple thromboses
  • thrombosis while anti-coagulated
115
Q

What factors can increase the risk of venous thrombosis?

A
  • Reduced anticoagulant proteins
  • Increased coagulant factors
    (increased activity due to activated protein C resistance)
116
Q

What can cause an increased platelet count?

A

myeloproliferative disorders

117
Q

What can cause reduced anticoagulant proteins ?

A

nephrotic disease

118
Q

What do protein C and S inactivate?

A
  • FVa
  • FVIIIa
119
Q

What are the anticoagulant proteins?

A
  • antithrombin
  • protein C
  • protein S
120
Q

What are the coagulant factors?

A
  • FVIII
  • FII
  • FV
121
Q

What does antithrombin inactivate?

A
  • FVIIa
  • FXa
122
Q

What deficiency puts you most at risk of a venous thrombosis?

A

antithrombin deficiency (25-50 odds ratio)

123
Q

What is the effect of abnormal FVa Lieden?

A

increased thrombotic activity

124
Q

Why is the vessel wall thought to have an effect on venous thrombosis?

A

many proteins are expressed on the endothelial surface and their expression changes in inflammation

125
Q

What is the change in blood flow that increases the risk of thrombosis?

A 
reduced flow (stasis) 
EG: surgery, long haul flight, and pregnancy
126
Q

What is the nature of the cause of venous thrombosis?

A

multi-causal - interacting genetic and acquired factors

127
Q

How do you prevent venous thrombosis?

A
  • assess and prevent risks
  • prophylactic anticoagulant therapy
128
Q

How do you reduce the risk of recurrence/extension of venous thrombosis?

A
  • lower procoagulant factors (warfarin, DOACs)
  • increase anti-coagulant activity (heparin)
129
Q

What are the risk factors for thrombosis?

A
  • age
  • obesity
  • thrombosis at a young age
  • multiple thromboses
  • thrombosis while anticoagulated
130
Q

What is heparin?

A
  • inactivates thrombin and factor X
  • via activating antithrombin III
  • IV administration
131
Q

What is low molecular weight heparin

A
  • same as heparin but only inhibits factor X
  • SC administration
132
Q

What is warfarin?

A
  • inhibits factor II, VII, IX and X
  • via inhibiting vitamin K reductase
  • oral
133
Q

What are direct oral anticoagulants?

A
  • directly inhibits thrombin or Xa
  • oral

BRS YR2 (67 decks)

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