Haemostasis Flashcards

1
Q

Why clot

A

to keep blood in and pathogens out

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2
Q

what is haemeostasis

A

physiological process that stops bleeding at the site of an injury whilst maintaining normal blood flow elsewhere

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3
Q

primary

A
  1. adhere
  2. activate
  3. aggregate
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4
Q

secondary

A

thrombin (Protease)cleaves circulating soluble fibrinogen into insoluble fibrin mesh

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5
Q
  1. adherence- endothelium releases what
A

von willebrand factor

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6
Q

1.adherence- where is von willebrand factor stored

A

Weibel-Palade bodies in endothelial cells

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7
Q

1.adherence - what does von willebrand bind to

A

exposed collagen

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8
Q

1.adherence- what do platelets express receptors for

A

collagen and functional fibrinogen receptors

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9
Q

1.adherence- what happens to platelets when bound

A

activated

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10
Q
  1. activation- what do platelets bind to
A

fibrinogen

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11
Q
  1. activation- what do platelets release after binding to fibrinogen
A

multiple pro activation signalling molecules e.g adenosine diphosphate (ADP) + thromboxane A2 (TXA2)

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12
Q
  1. Aggregation
A

linking of platelets- activated by other platelets, dont need to see wound

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13
Q

Secondary- what is the sub-endothelial trigger for coagulation cascade

A

tissue factor

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14
Q

Amplification- each activated factor activates more of the next (5)

A
  1. activated platelet(signalling molecules +fibrinogen)
  2. initial trickle of thrombin
  3. Tissue factor(TF)- expressed by sub endothelial cells- activates coagulation cascade to initiate minor burst of heamostasis
  4. Factor 7a binds to TF which leads to conversion of prothrombin- thrombin
  5. thrombin activates receptors on platelets + endothelium -amplifying + initiating release of stored von willebrand from cells
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15
Q

Secondary(amplification)- what activates coagulation cascade

A

tissue factor

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16
Q

Secondary(amplification)- what binds to TF

A

Factor 7a

17
Q

Secondary(amplification)- binding of factor 7a to TF leads to what

A

conversion of prothrombin to thrombin

18
Q

Secondary(amplification)- what does thrombin activate

A

receptors on platelets and on endothelium- release of more von willebrand

19
Q

Secondary- what two cofactors does thrombin activate

A

factor 8a and 5a

20
Q

what are the two calcium ion dependant complexes on the surface of platelets called

A
  1. prothrombinase complex (factor 5a)

2. tenase complex (factor 4a)

21
Q

what does the prothrombinase complex (factor5a) accelerate the production of

A

factor 5a

22
Q

what does the tenase complex (factor 4a) accelerate the production of

A

thrombin

23
Q

what is heamophilia

A

failing to clot

24
Q

thrombosis

A

clotting in the wrong place e.g arterial(stroke)

venous(DVT)

25
Q

disseminated intravascular coagulation(DIC)

A

whole body clots- sepsis

depletion of clotting factors and platelets lead to bleeding

26
Q

why is coagulation activated during sepsis

A

can be beneficial during infections since proteins are necessary for eradication of invading pathogens

27
Q

what is the containment hypothesis

A

coagulation activation contributes to pathogen clearance by forming a physical barrier facilitating pathogen clearance by immune cells