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Molecular Basis Of Disease > Disorders Of Blood Coagulation > Flashcards

Disorders Of Blood Coagulation Flashcards

1
Q

Why are blood clots important?

A

Blood loss is stopped by formation of. Plug composed of platelets and fibrin

Must remain localised

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2
Q

What is haemostasis?

A

Endothelium in blood vessels normally maintains a anticoagulant surface

When Damage to vessel wall triggers clotting Causes Platelets and fibrinogen aggregate forming a mesh

Primary and secondary haemostasis occur independently at the same time

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3
Q

What occurs during PRIMARY haemostasis?

A
  1. Endothelium continuously releases small amount of Von Willabrand factor, which circulates in the blood. - - Endothelial cells store Von willabrand factor in Weibel-palade bodies for release when appropriately stimulated.
  2. If collagen becomes exposed to blood due to endothelial damage, Von willabrand factor binds to it
  3. Platelets express receptors for both collagen and Von willabrand factor.
  4. When von willabrand factor and collagen bind to thee receptors platelets become activated
  5. Activated platelets express functional fibrinogen receptor, which are required for aggregation
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4
Q

What occurs during SECONDARY haemostasis?

A
  1. Tissue factor is expressed by most sub-endothelial cells
  2. Tissue factor activates the coagulation cascade to initiate a minor burst of thrombin that can then be amplified
  3. Tissue factor binds to factor 7a
  4. Factor 7a then activates factor 10a
  5. Factor 10a then induces the initial trickle of thrombin from prothrombin
  6. Thrombin activates receptors on platelets as well as endothelial cells - amplifying platelet aggregation and initiating release of stores Von willabrand factor from endothelial cells.
  7. Thrombin activates 2 co factors (8a + 5a) which form calcium ion dependent complexes on the surface of platelets with 10a - this complex accelerates the production of factor 10a and thrombin
  8. The increase in the production of thrombin contributes considerably to the process where thrombin will convert fibrinogen to the fibrin mesh.
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5
Q

Describe how thrombin is produced?

A

Prothrombase is converted to thrombin using tenase

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6
Q

What is fibrinolysis?

A
  1. Plasminogen is activated to plasmin (proteolitic enzyme) by plasminogen activator (t-PA)
  2. Plasmin degrades the fibrin mesh to fibrin degradation products (eg. D dimer)1 which can be cleared.

This prevents blood clots from growing and becoming problematic.

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7
Q

What is antithrombin?

A

A serpin (serine protease inhibitor) found on heparin binding sites of endothelial cells
It inhibits the activity of thrombin and factor 10a.

Activity greatly enhanced by heparin binding sites on endothelial cells
- it’s HEPARAN binding domain is the basis of the anticoagulant activity of heparin
- heparin enhances the activity of anticoagulant

Major checkpoint to inhibit coagulation

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8
Q

What are examples of natural anticoagulants in the body?

A
  • antithrombin
  • protein C and protein S
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9
Q

How do protein C and protein S function to prevent coagulation?

A

Natural anticoagulant plasma protiens

Plasma C:
- activated by thrombin (bound to thrombomodulin) on endothelial cells
- form activated protein C (APC)
- degrades cofactors 8a and 5a

Plasma S:
- APC cofactor
- helps complex bind to cell surfaces

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10
Q

What molecular components of blood clotting are effected in blood clotting disorders?

A

Coagulation proteins

Platelets

Endothelium

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11
Q

What is haemophilia?

A

Failure to-clot leading to haemorrhage

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12
Q

What are the three causes of haemophilia?

A
  • mutations in coagulation factors (haemophilia A and B)
  • platelet disorders (Von willebrand disease)
  • collagen abnormalities (fragile blood vessels and bruising)
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13
Q

What is thrombophillia?

A

Excessive clotting leading to thrombosis

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14
Q

What are the 2 causes of thrombophillia?

A
  • inherited: mutations in coagulation factors (DVT)
  • acquired: malignancy increases clotting factors (DVT)
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15
Q

What is disseminated intravascular coagulation (DIC)?

A

Whole body clots

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16
Q

What are the 2 causes of DIC?

A
  • infection
  • depletion of clotting factors and platelets leads to bleeding
17
Q

Where do the mutation occur for bleeding disorders?

A

Haemophilia A - mutated factor 8a (80% so common)

Haemophilia B - mutated factor 9a (20% so less common)

Von willebrand disease - inherited defect/deficiency in vWF

18
Q

How does factor 5 Leiden mutations lead to excessive clotting?

A
  • natural anticoagulant pathway of protein C cannot inhibit the activity of factor 5
  • resistance to APC
  • therefore factor 5a is not inactivated
  • increased risk of DVT
19
Q

How does antithrombin deficiency lead to excessive clotting?

A
  • Thrombin, Factor 10a and 9a can not be inactivated
  • increased risk of DVT
20
Q

How can mutations in Protein C and S lead to excessive clotting?

A

Cannot inactivate factors 5 and 8

Increased risk of DVT

21
Q

What factors causes deep vein thrombosis?

A

Alterations in the constituents of the blood

Changes in normal blood flow

Damage to the endothelial layer

22
Q

What does Virchow’s triad consist of?

A

Stasis

Vessel wall injury

Hyper-coagulability

23
Q

What are the symptoms of deep vein thrombosis?

A
  • pain and tenderness of veins
  • limb swelling
  • increased skin temperature
  • superficial venous distension
  • skin discolouration
24
Q

What is deep vein thrombosis?

A

When excessive coagulation causes blockage of deep veins.

Increases the risk of pulmonary embolism (clot moves to the lungs) - higher risk when clot is above the knee

25
Q

What occurs during Disseminated intravascular coagulation (DIC)?

A

Sepsis (bodies response to infections injuries it’s own tissues and organs)

Depletion of clotting factors and platelets leads to bleeding

26
Q

What is the role of anticoagulants?

A

To prevent more coagulation form happeneing

Eg. Warfarin, heparin, direct oral anticoagulants (DOAC)

27
Q

What is the role of thrombolytics/fibrinolytic reverse?

A

Degrade blood clots

Eg. Plasminogen activators (tPA), streptokinase

28
Q

What investigations can be done for venous thromboembolism in pre-clinical treatment?

A
  • clotting screening (prothrombin time, thrombin time) - COVERED IN YEAR 1
  • full blood count
  • renal screen
  • liver function tests (in suspicion of liver disease)
29
Q

What treatments are given to those with DVT?

A

Anticoagulants
- immediate anticoagulant effect
- heparin or warfarin
- DOACs (eg. danigatran and pivaroxaban)

30
Q

What treatments are given for PE (pulmonary embolism)?

A

Thrombolysis
- Alteplase (tissue plasminogen activator)
- streptokinase
- followed by anticoagulant to prevent reassurance

31
Q

What bleeding complications can occur from anticoagulants?

A
  • small haemorrhages
  • nose bleeds
  • bruising at elbow
  • bleeding in the brain (cerebrum) - can cause strokes

Molecular Basis Of Disease (32 decks)

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