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MBD > Disorders Of Blood Coagulation > Flashcards

Disorders Of Blood Coagulation Flashcards

1
Q

Why is blood clotting a good thing?

A
  • Stops bleeding at the site of injury
  • Keeps blood in and pathogens out
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2
Q

What activates clotting?

A

Endothelium in blood vessels normally maintains an anticoagulant surface- when this is broken, collagen is exposed which activates clotting

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3
Q

Why must clotting remain localised?

A

Systemic blood clots not wanted

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4
Q

What is involved in primary haemostasis?

A
  • Platelet adhesion, aggregation, activation
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5
Q

What is involved in secondary haemostasis?

A

Activation of fibrin formation through the clotting cascade

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6
Q

What occurs in the vessels when there is injury?

A
  • Endothelium in blood vessels normally maintains an anticoagulant surface
  • Circulating factors e.g fibrinogen precursor of fibrin in the blood in the inactive form.
  • Damage to vessel wall triggers primary and secondary haemostasis.
  • Injury exposes collagen to come into contact with blood components to activate clotting.
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7
Q

What happens in primary haemostasis?

A
  • If collagen becomes exposed to blood, von willebrand factors bind to it
  • Von willebrand factors bind to platelets from blood and activate them
  • Activated platelets express functional fibrinogen receptors which are required for aggregation
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8
Q

What happens in secondary haemostasis?

A
  • Tissue factor activates the coagulation cascade to initiate a minor burst of thrombin
  • Factor VIIa binds to tissue factor which ultimately leads to conversion of prothrombin to thrombin
  • Thrombin activates receptors on platelets and endothelium → amplification of platelet aggregation and release of von willebrand factors
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9
Q

What is the amplification step of secondary haemostasis?

A
  1. Thrombin activates two cofactors, Factor VIIIa and factor Va
  2. This subsequently forms calcium ion-dependent complexes on the surface of platelets with factor IXa (tenase complex) which activates factor Xa
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10
Q

What does the tenase complex do?

A

Accelerate production of factor Xa

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11
Q

What does the prothrombinase complex do?

A

Activate thrombin

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12
Q

What is plasminogen?

A

Plasminogen is a precursor for plasmin

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13
Q

What is plasmin?

A
  • Plasmin is a potent proteolytic enzyme.
  • Plasmin breaks down fibrin into fibrin fragments
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14
Q

What is an example of fibrin degredation products?

A
  • D-dimer
  • D-dimer is a marker in disorders
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15
Q

What is fibrinolysis?

A

Fibrinolysis is the same as thrombolysis

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16
Q

What is the process of fibrinolysis?

A
  1. Plasminogen → Plasmin by tissue plasminogen activator (tPA)
  2. Plasmin then degrades the fibrin mesh → fibrin degredation products
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17
Q

Why are natural anticoagulants important?

A
  • Natural anticoagulants are important to keep coagulation in check.
  • Too much coagulation is detrimental so its vital to have anticoagulant pathways to prevent too much thrombin formation
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18
Q

What is thrombin responsible for activating?

A

Thrombin is responsible for activation of:

  • von Willebrand factor from endothelial cells
  • factors Xa and IXa
  • platelets
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19
Q

Where is tissue plasminogen activator found?

A

Endothelial cells

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20
Q

Where is antithrombin found?

A

On the surface of endothelial cells by binding to heparan binding sites on the endothelial cell surface, this binding to heparan greatly enhances antithrombin activity

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21
Q

What is heparin and what does it do?

A

An anti-coagulant drug that is similar in structure to heparan to enhance the activity of antithrombin

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22
Q

What are protein C and S?

A

Natural anticoagulant plasma proteins

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23
Q

What is protein C activated by?

A

Thrombin bound to thrombomodulin on endothelial cells

24
Q

What does protein S do?

A

Protein S allows for APC to bind to other molecules e.g. platelets etc.

25
Q

What does APC do?

A

Degrades cofactors FVa and FVIIIa in the coagulation pathway

26
Q

What are three blood clotting disorders?

A
  • Haemophilia
  • Thrombophilia
  • Disseminated intravascular coagulation
27
Q

What is haemophilia?

A

Failure to clot leading to haemorrhage

28
Q

Describe some of the different ways that one can have haemophilia

A
  • Mutations in coagulation factors (haemophilia A or B)
  • Platelet disorders (von Willebrand disease)
  • Collagen abnormalities (fragile blood vessels and bruising)
29
Q

What are haemophilia A and B ?

A
  • Mutations in coagulation factors
30
Q

How common is is haemophilia B and what mutation causes it?

A
  • Mutated clotting factor 9
  • 20% of haemophilia cases
31
Q

How common is is haemophilia A and what mutation causes it?

A
  • Mutated clotting factor 8
  • 80% of haemophilia cases
32
Q

What is von willebrand disease categorised as?

A

Platelet disorder

33
Q

What do collagen abnormalities cause?

A

Fragile blood vessels and bruising

34
Q

What is thrombophilia?

A

Excessive clotting leading thrombosis

35
Q

Describe some different ways that one can have thrombophilia

A
  • Inherited – mutations in coagulation factors
  • Acquired – malignancy increases clotting factors
36
Q

What causes inherited thrombophilia?

A

Mutations in coagulation factors

37
Q

What causes acquired thrombophilia?

A

Malignancies such as cancer may increase clotting factors

38
Q

What is disseminated intravascular coagulation (DIC)?

A

Systemic clotting (Whole body clots)

39
Q

Where does bleeding occur in haemophilia vs vWF disease?

A

Haemophilia - in the joints like the knees

vWF - (is milder and often just treated by being careful and lifestyle choices) affects the mucus membranes so there may be bleeding around the gums

40
Q

How does Factor V Leiden Mutation lead to excessive clotting?

A

Resistance to APC → FVa not activated → increased risk of DVT (deep vein thrombosis)

41
Q

How does antithrombin deficiency lead to excessive clotting?

A
  • Thrombin, IXa and FXa are not inactivated – clotting increases
  • Increases risk of DVT
42
Q

What are some causes of excessive clotting?

A
  • Factor V leiden mutation
  • Antithrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
43
Q

What does DVT development depend on?

A
  • Alterations in the blood constituents
  • Changes in normal blood flow
  • Damage to the endothelial layer
44
Q

What are the symptoms of DVT?

A
  • Pain and tenderness of veins
  • Limb swelling
  • Superficial venous distension
  • Increased skin temperature
  • Skin discolouration
45
Q

What are the risks with DVT?

A
  • If the clot is above the knee it is significantly more likely to embolise
46
Q

When does disseminated intravascular coagulation occur and why?

A
  • Occurs in infection and sepsis (body’s response to an infection injures its own tissues and organs)
  • So much coagulation that there is depletion of clotting factors and platelets leads to bleeding
47
Q

What happens in disseminated intravascular coagulation (DIC)?

A

Depletion of clotting factors and platelets leading to bleeding so there is coagulation and bleeding occurring at the same time

48
Q

What do anticoagulants do?

A

Prevent more clotting

49
Q

What do thrombolytics/ fibrinolytics do?

A

Reverse clotting

50
Q

Give some examples of anticoagulants

A
  • Warfarin
  • Heparin
  • Direct oral anticoagulants (DOACs)
51
Q

Give examples of thrombolytics/fibrinolytics

A

Plasminogen activators : TPA, streptokinase

52
Q

What does VTE stand for?

A

Venous thrombus embolism

53
Q

What pre-treatment investigations can you give for VTE?

A
  • Clotting screen
  • FBC
  • Renal screen
  • Liver function tests
54
Q

What does the clotting screen show?

A
  • Prothrombin time
  • Partial thromboplastin time
  • Thrombin time
55
Q

What are the treatments for DVT?

A

Anticoagulants

56
Q

What are examples of DOACs?

A
  • Rivaroxaban and apixaban
  • Dabigatran
57
Q

What are some bleeding complications from anticoagulants?

A
  • Anything from nosebleed up to intercranial haemorrhage in severe cases

MBD (23 decks)

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