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[MBD] NoNa > Disorders of blood coagulation > Flashcards

Disorders of blood coagulation Flashcards

1
Q

Why does blood clot ?

A

Blood clotting = Defence mechanism following injury/trauma (keep blood in,pathogens out)

Blood loss is stopped through formation of a platelet+fibrin plug

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2
Q

What are the 2 main processes of Haemostasis?

A

Primary Haemostasis

Secondary Haemostasis

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3
Q

Describe blood clotting simply

A
  • Blood vessel endothelium normally maintains an anticoagulant surface
  • Platelets and fibrinogen circulate in the blood (inactive form)
  • Damage to vessel wall = exposes subendothelial collagen to blood = collagen attracts platelets = activates clotting
  • Platelets aggregate at blood vessel injury site + fibrin mesh forms
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4
Q

Describe primary haemostasis

A

Primary Haemostasis = Platelet Adhesion, Activation and Aggregation:

  1. Endothelium continuously releases little vWF = vWF circulates in blood.
    Endothelial cells also store von Willebrand factor in Weibel-Palade bodies (storage granules) for release when stimulated.
  2. Damage to blood vessel wall = endothelium damage = collagen becomes exposed to blood. von Willebrand Factor binds to exposed collagen.
  3. Platelets express receptors for both collagen and von Willebrand Factor. Platelets become activated when both these proteins bind to platelet.
    Activated platelets express fibrinogen Rs (required for later aggregation).
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5
Q

Describe secondary haemostasis

A

Secondary haemostasis = Activation of fibrin formation in clotting cascade

  1. Tissue factor expressed by nearly all sub-endothelial cells activates the coagulation cascade to initiate a minor burst of thrombin.Factor FVIIa binds to Tissue factor which leads to the conversion of prothrombin to thrombin.
  2. Thrombin activates receptors on platelets as well as endothelium amplifying platelet aggregation and initiating release of stored von Willebrand factor from endothelial cells.
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6
Q

Describe the amplification of Thrombin

A

Thrombin activates two cofactors :Factor VIIIA and Factor Va which form calcium ion dependent complexes on the surface of platelets with Factor IXa (tenase complex) and Factor Xa (prothrombinase complex).

2.These complexes will accelerate production of Factor Xa and thrombin. This is the amplification stage of the coagulation cascade.
\the greatly increased production of thrombin via tenase and prothrombinase contributes to the process.Thrombin will convert fibrinogen to the fibein mesh.

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7
Q

What is Fibrinolysis?

A

This is the breakdown of the fibrin in blood clots

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8
Q

Describe Fibrinolysis

A
  1. Plasminogen inactivated to plasmin by tissue plasminogen activator t-PA(expressed on surface of endothelial cells)
  2. Plasmin degrades the fibrin mesh to fibrin degradation products which can be cleared
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9
Q

Describe the Antithrombin natural anticoagulant pathway

A

Too much coagulation can be a problem.

Antithrombin (AT) is a serpin (serine protease inhibitor).
Its activity is enhanced by binding heparan binding sites on endothelial cells.

Major checkpoint to inhibit coagulation (thrombin) Ixa,Xa.Its heparan binding domain is the basis of the anticoagulant activity of heparin which increases the activity of ATIII.

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10
Q

Describe the Protein C/S anticoagulant pathway

A

Protein C/S are natural anticoagulant plasma proteins.
Protein C is activated by thrombin bound to thrombomodulin(TM) on endothelial cells to form activated protein C (APC).

Protein S is an APC cofactor which helps binding to cell surfaces for e.g platelets. APC degrades cofactors FVa and FVIIIa(part of tenase and prothrombinase complex).

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11
Q

What are three disorders of blood coagulation?

What are the three components in which defects occour ?

A

Haemophilia
Thrombophilia
Disseminated intravascular coagulation

  • Coagulation proteins
  • Platelets
  • Endothelium
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12
Q

Describe Haemophilia

A

Failure to clot leading to haemorrhage

  • Mutations in coagulation factors (haemophilia A/B)
  • Platelets disorders(Von willebrand disease-required to activate platelets in primary haemostasis)
  • Collagen abnormalities(fragile blood vessels and bruising)
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13
Q

Describe Thrombophilia

A

Excessive clotting leading to thrombosis

  • Inherited (Mutations in coagulation factors(DVT)
  • Acquired(Malignancy increases clotting factors (DVT)
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14
Q

Describe dissemintated intravascular coagulation (DIC)

A

This is whole body clots
Infection
Depletion of clotting factors and platelets leads to bleeding.
This can also happen in sepsis when the body’s response to an infection injures its tissues and organs

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15
Q

Describe the mutations of Haemophilia

A 
Haemophilia A (80% of cases)
Mutated FVIII(8)
Haemophilia B 
Mutated FIX (9)
Von Willebrand disease 
Inherited defect/deficiency in vWF (No platelet adhesion/aggregation)
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16
Q

What are some symptoms of Haemophilia?

A

Massive haemorrhages

Gross swelling from acute haemarthroses(bleeding into the joints) of the knee joints

17
Q

What are some symptoms of Von Willebrand disease?

A

It affects mucous membranes

Bleeding gums, but bleeding can vary in severity

18
Q

What mutations can lead to excessive clotting ?

A
  1. Factor V Leiden mutation
    This can lead to APC resistance which means that
    FVa is not inactivated
    Increases risk of DVT
  2. Antithrombin deficiency
    Thrombin, IXa and FXa are not inactivated
    This increases risk of DVT.

3.Protein C/S deficiney
Increase DVT risk

19
Q

What is Virchow’s Triad ?

A

These are Thrombosis causes:

  • Vessel Wall injury
  • Hypercoagulability
  • Stasis (Imobility)

Development of a venous thrombus can depend on :

  • Alterations in the constituents of the blood
  • Changes in normal blood flow
  • Damage to the endothelial layer
20
Q

What are the symptoms of Deep Vein thrombosis ?

A 
This can cause swelling and skin changes 
Pain and tenderness of veins 
Limb swelling
Superficial venous distention 
Increased skin temperature
Skin discoloration
Increased risk of pulmonary embolism
(All causes are due to venous drainage obstruction)
21
Q

Describe the types of management of thrombosis

A

Anti-coagulants
(Warfarin, Heparin, Direct oral anti-coagulants (DOACS)

These prevent clots from becoming worse.

Thrombolytics/Fibrinolytics reverse:
Plasminogen activators, tPA streptokinase
(degrade the clots)

22
Q

What are some investigations of pre-treatments?

A 
Clotting screen 
-Prothrombin time
-Partial thromboplastin time
-Thrombin time 
Full blood count
Renal screen 
Liver function test 
-If clinical suspician of liver disease
23
Q

What are some direct treatments of VTE?

A 
DVT:Anticoagulant 
-Immediate anticoagulant effect 
-Heparin/Wafarin 
-DOACs
(Rivaroxaban apicaban FXa inhibitors)
(Dabigatran thrombin (FIIa inhibitors)
-PE:thrombolysis 
-Alteplase (Tissue plasminogen activator)
(Streptokinase 
Followed by anticoagulant to prevent recurrence
24
Q

Insufficient clotting =

Excessive clotting =

A

Insufficient clotting = haemorrhage

Excessive clotting = thrombosis

25
Q

Blood coagulation must be …………. bc we don’t want ……….. blood clots

A
  • localised

- systemic

26
Q

Endothelium in blood vessels normally maintains ……………………….. surface

A

an anticoagulant

27
Q

………………….circulate ready to go.

A

Platelets and fibrinogen (inactive fibrin precursor)

28
Q

Damage to vessel wall triggers ………….

A
  • Damage to vessel wall triggers clotting (primary + secondary haemostasis)
  • Endothelium in blood vessels normally maintains an anticoagulant surface
  • Injury exposes collagen to come into contact with blood components = blood components activate clotting (primary + secondary haemostasis)
29
Q

……… cells are important in clotting + anticoagulant pathways

A

endothelial cells are important in clotting + anticoagulant pathways

30
Q

What is the difference between haemostasis and fibrinolysis?

A
31
Q

What are primary and secondary haemostasis?

A
32
Q

What is the cell-based model of coagulation?

A
33
Q

What is antithrombin?

A
34
Q

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

A
35
Q

What defects lead to haemophilias A and B?

A
36
Q

What is von Willebrand disease?

A
37
Q

Explain resistance to activated protein C and how it leads to increased risk of DVT.

A
38
Q

Give examples of direct oral anticoagulants

A
39
Q

Primary haemostasis and secondary haemostasis occur ……………………..

A

simultaneously

[MBD] NoNa (28 decks)

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