Haemostasis Flashcards

1
Q

what are the requirements of haemostasis?

A
  • permanent state of readiness
  • prompt response
  • localised response
  • protection against unwanted thrombosis
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2
Q

what are the four different components of a normal haemostatic system

A
  • formation of a platelet plug
  • formation of a fibrin clot
  • fibrinolysis
  • anticoagulant defences
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3
Q

what is primary haemostasis ?

A

formation of a platelet plug

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4
Q

what is secondary haemostasis?

A

formation of a fibrin clot

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5
Q

where do platelets come from?

A

they bud off from the cytoplasm of megakaryocytes in the bone marrow and enter the blood stream

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6
Q

what is the life span of a platelet ?

A

7-10 days

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7
Q

what is involved in the process of platelet adhesion?

A

when there is damage to the endothelial wall, this exposes collagen and so for whatever reason the endothelium released a factor called Von Willerbrand factor (VWF), platelets in the blood have receptors to these proteins and so bind with them at the site injury

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8
Q

what is meant by platelet aggregation

A

when the platelets bind at the site of injury they secrete various chemicals which leads to lots more platelets aggregation at this site of injury (which then plugs the hole and we achieve primary haemostasis)

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9
Q

what causes failure of the formation of the platelet plug?

A
  • vascular ie old people don’t have as much collagen in their endothelial walls and so not a lot of VWF is released
  • thrombocytopenia
  • reduced platelet function (drug use)
  • Von Willerbrand factor ie Von Willerbrand’s is a disease in which your blood does not clot properly/continuous bleeding
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10
Q

what are the consequences of failure of primary haemostasis?

A
  • spontaneous bruising and purpura (small purple/blue dots that don’t blanch)
  • mucosal bleeding
  • intracranial haemorrhage
  • retinal haemorrhage
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11
Q

how is fibrin clot produced

A

> clotting factors VIIa , V , Xa and VIII and IXa sit on top of the phospholipid bilayer of the platelet
INITIATION:
when there is cell injury - as well as VWF - the endothelium releases Tissue Factor (TF) which activates clotting factor VII, TF and VII then activates V and Xa
activated V/Xa is called Taney’s complex and this activates prothrombin to turn into thrombin
PROPAGATION:
thrombin cleaves fibrinogen into fibrin
however we don’t get a lot of TF released and so this mechanism alone wouldn’t produce enough fibrin
AMPLIFICATION:
so thrombin activates VIII/IXa which then goes on to activate more V/Xa which then activates more prothrombin etc

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12
Q

what are the causes of failed secondary haemostasis?

A
  • single clotting factor deficiency (usually hereditary ie haemophilia)
  • multiple clotting façtor deficiencies (usually acquired ie liver failure)
  • increased fibrinolysis (usually as part of complex coagulopathy)
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13
Q

what is fibrinolysis?

A

the breaking down of a fibrin clot

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14
Q

what is involved in the process of fibrinolysis?

A

> fibrin is broken down by an enzyme called plasmin into fibrin degradation products (FDPs)
**FDPs become D-dimers
the precursor for plasmin is plasminogen and it is activated by Tissue Plasminogen Activator (tPA)
*can use tPA therapeutically

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15
Q

what are the consequences of failure of secondary haemostasis?

A

-there is no characteristic clinical syndrome
-pattern of bleeding depends on: the number of abnormalities
and the clotting factors involved

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16
Q

what is anti-thrombin ?

A

it is an anti-coagulant serine protease inhibitor

-once haemostasis is achieved anti-thrombin with inactive thrombin and stop the formation of fibrin

17
Q

what are protein C and protein S ?

A

anticoagulants that switch of clotting factors VIII and V respectively

> these two proteins are activated when thrombin binds to thrombomodulin (it does this when haemostasis has been achieved)

18
Q

what are some venous thrombotic events

A

DVT

PE

19
Q

what are some arterial thrombotic events

A

coronary, cerebral, peripheral

20
Q

what are the three components of Virchow’s Triad

A
  • stasis
  • vessel wall
  • hypercoagulability