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omgmbd > L14: Disorders Of Blood Coagulation > Flashcards

L14: Disorders Of Blood Coagulation Flashcards

1
Q

Why does clotting occur?

A

→Blood loss is stopped by formation of a plug composed of platelets and fibrin

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2
Q

What does the endothelium maintain in blood vessels?

A

→maintains an anticoagulant surface

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3
Q

What are the two main processes of haemostasis?

A

→primary and secondary

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4
Q

What is primary haemostasis of clotting?

A

→when platelet adheres, activation

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5
Q

What is secondary haemostasis of clotting?

A

→activation of fibrin formation

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6
Q

Describe primary haemostasis

A

→Endothelial cells also store von Willebrand Factor in Weibel-Palade bodies for release when appropriately stimulated
→If collagen becomes exposed to blood von Willebrand Factor binds to it
→Platelets express receptors for both collagen and von Willebrand Factor and become activated when these proteins bind to them
→Activated platelets express functional fibrinogen receptors, which are required for aggregation.

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7
Q

Describe secondary haemostasis

A

→Tissue factor (TF), activates the coagulation cascade to initiate a minor burst of thrombin

→Factor FVIIa binds to Tissue Factor, which ultimately leads to conversion of prothrombin to thrombin

→Thrombin activates receptors on platelets and endothelium
→amplifies platelet aggregation and initiating release of stored von Willebrand Factor from endothelial cells.

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8
Q

Which cell express tissue factor?

A

→by nearly all sub-endothelial cells

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9
Q

When would collagen become exposed?

A

→because the endothelium is damaged

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10
Q

Describe the amplification process in clotting

A

→Thrombin activates Factor VIIIa and Factor Va
→subsequently form calcium ion-dependent complexes on the surface of platelets with Factor IXa and Factor Xa
→accelerate production of Factor Xa and thrombin, respectively

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11
Q

Which factors does thrombin activate?

A

→Factor VIIIa and Factor Va

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12
Q

Where are the calcium dependent complexes found?

A

→surface of platelets with Factor IXa

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13
Q

What is the tenase complex?

A

→Factor IXa and Factor VIIIa

→substrate is Factor X

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14
Q

What is the prothrombinase complex?

A

→Factor Xa

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15
Q

What does thrombin convert?

A

→convert fibrinogen to the fibrin mesh

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16
Q

Describe fibro lysis

A

→Plasminogen in activated to plasmin by tissue plasminogen activator, t-PA
→Plasmin degrades the fibrin mesh to fibrin degradation products which can be cleared

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17
Q

What is plasmin?

A

→proteolytic and very potent

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18
Q

What is antithrombin?

A

→a serpin

serine protease inhibitor

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19
Q

How is antithrombin activity enhanced?

A

→by binding heparan binding sites on endothelial cells

20
Q

What is the role of antithrombin?

A

→checkpoint to inhibit coagulation (thrombin), IXa, Xa)

21
Q

What does heparin mimic in heparan?

A

→binding domain

→increases the activity of ATIII

22
Q

What are the natural anticoagulants?

A

→antithrombin

→protein C and S

23
Q

What is Protein C activated by?

A

→by thrombin bound to thrombomodulin (TM) on endothelial cells

24
Q

What is protein S?

A

→APC cofactor which helps binding to cell surfaces

25
Q

Which factors degrades APC?

A

→degrades cofactors FVa and FVIIIa

26
Q

What is haemophillia?

A

→- failure to clot leading to haemorrhage

27
Q

What are the causes of haemophillia?

A

→Mutations in coagulation factors (haemophilia A and B)

→Platelet disorders (von Willebrand disease)

→Collagen abnormalities (fragile blood vessels and bruising)

28
Q

What are the causes of thrombophillia?

A

→Inherited: mutations in coagulation factors (DVT)

→Acquired: malignancy increases clotting factors (DVT)

29
Q

What is DIC?

A

→Disseminated intravascular coagulation
→ whole body clots
→So much coagulation that clotting factors become depleted

30
Q

What are the causes of DIC?

A

→Infection

→Depletion of clotting factors and platelets leads to bleeding

31
Q

What are examples of bleeding disorders?

A 
→von Willebrand disease
Inherited defect/deficiency in vWF
→Haemophilia B (20%)
Mutated FIX
→Haemophilia A (80%)
Mutated FVIII
32
Q

What are clinical symptoms of of heamophillia?

A

→bleeding in the joints

33
Q

What are clinical features of von Willebrand disease?

A

→mucous membranes bleeding

34
Q

What does Factor V Leiden mutation lead to?

A

→Resistance to APC
→FVa is not inactivated
→Increases risk of DVT

35
Q

What does antithrombin deficiency lead to?

A

→Thrombin, IXa and FXa are not inactivated

→Increases risk of DVT

36
Q

What does protein C and S deficiency lead to?

A

→Protein C deficiency

→Protein S deficiency

→Increases risk of DVT

37
Q

What are the three parts of Virchow’s triad?

A

→stasis
→vessel wall injury
→hypercoagulability

38
Q

What are the symptoms of DVT?

A 
→Pain & tenderness of veins
→Limb swelling 
→Superficial venous distension
→Increased skin temperature 
→Skin discoloration
39
Q

What mutations/deficiency can lead to excessive clotting?

A

→Factor V Leiden mutation
→Antithrombin deficiency
→Protein C deficiency
→Protein S deficiency

40
Q

What are the pre-treatment investigations of VTE?

A

→Clotting screen

→Full blood count

→Renal screen

→Liver function tests

41
Q

What tests are involved in clotting screen?

A

→Prothrombin time
→Partial thromboplastin time
→Thrombin time

42
Q

What are the treatments for DVT?

A

→Immediate anticoagulant effect

→Heparin or warfarin

→DOACs

43
Q

Give two examples of DOACs and what they inhibit

A

→Rivaroxaban, apixaban (FXa inhibitors)

→Dabigatran (thrombin (FIIa) inhibitor)

44
Q

What are the treatments for pulmonary embolism?

A

→Alteplase (tissue plasminogen activator)

→Streptokinase

→Followed by anticoagulant to prevent recurrence

45
Q

What can result from excess anticoagulants?

A

→bleeding in the brain, arm or eyes

46
Q

What are DOACs?

A

→direct oral anticoagulants

omgmbd (29 decks)

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