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Cardiovascular System > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is the haemostatic system

A

cascade/amplification system that stops the body from bleeding.
Haemostasis is a state of equilibrium between fibrinolytic factors, anticoagulant proteins, coagulation factors and platelets

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2
Q

What are some factors associated with haemostasis

A

Von Willebrand factor

Platelets

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3
Q

What state are factors and co factors at rest

A

They are separated

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4
Q

Describe VWF

A

Very large and sticky protein with multiple binding sites

Largest protein in the blood

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5
Q

Describe platelets and their receptors

A 
Fragments of megakaryocytes
Half of 10 days
Localise and accelerate reactions
GP1a
Thromboxane receptors
Purine receptors
VWF receptors
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6
Q

Explain the process of platelet activation

A
  1. change in shape
  2. phospholipid is exposed
  3. new or activated proteins are presented on the surface e.g. GpIIb/IIa
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7
Q

Explain the process of platelet plug formation/primary haemostasis

A
  1. Damaged vessel wall
  2. The blood meets collagen and tissue factor outside the vessel
  3. VWF becomes stretched out across the damaged wall
  4. Platelets are captured when they roll by and attach to the VWF via their receptors
  5. Fibrinogen release to form the primary platelet plug
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8
Q

How do platelets bind

A

binds to VWF via Gp1b𝛼
Secondary binding to collagen via GpVI
Initiates activation
Aggregation with other platelets via GpIIb and fibrinogen
Ca2+ efflux
Granules in the collagen molecule degranulate to release VWF (alpha) and ADP (Dense)
Thromboxane A2 release

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9
Q

Why are tissue factors and collagen outside sub endothelial tissue

A

Prevent constant activation of factors and co-factors

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10
Q

What is required for primary haemostasis

A

Collagen
Platelets
VWF (initiator)

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11
Q

What is the limitation of solely using primary haemostasis

A

Can only be used for small vessels as large vessels require stabilisation (fibrin)

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12
Q

Describe secondary haemostasis

A

coagulation and formation of a fibrin mesh
Amplifies the initial stimulus to produce a burst of thrombin
Thrombin converts soluble fibrinogen into insoluble fibrin
cross-linked fibrin stabilises the primary platelet plug

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13
Q

What is secondary haemostasis triggered by

A

Tissue factor

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14
Q

What are some sites of clotting factor and fibrinolytic factors + inhibitors synthesis

A

liver
endothelial cells (VIII, VWF)
megakaryocytes

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15
Q

Describe clotting factor, fibrinolytic factor and inhibitor synthesis

A

VIIa circulates the blood
Circulates the blood and converts zymogens to proteinases Fxa
Thrombin is produced, activation FV and FVIII
FXI converted to FIXa

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16
Q

Where is the activation of FXII to FXIIa used

A

in vivo reaction used in diagnostic test

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17
Q

What is the function of thrombin

A

A burst of thrombin is essential, generating a stronger, denser clot more resistant to fibrinolysis

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18
Q

Describe thrombin action

A

Activates FXIII which cross link fibrin so it is more resistant to fibrinolysis
Activates TAFI, an inhibitor of fibrinolysis

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19
Q

Why is it important to control FVIIa generation

A

A small amount of FVIIa will produce a large amount of thrombin

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20
Q

Compare direct to indirect inhibition of thrombin generation

A

direct - antithrombin uses an inhibitor or thrombin and other clotting proteinases + TFPI in the initiation phase
indirect - inhibition of thrombin generation by protein C anticoagulant pathway

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21
Q

Describe antithrombin

A

Direct inhibitor of thrombin + proteinases
XIa. IXa. Xa. IIa (thrombin)
Complex from Iia, heparin and AT

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22
Q

Explain how protein C inhibits thrombin generation

A
  1. Thrombomodulin binds to free thrombin
  2. Thrombomodulin redirects activity from fibrinogen to protein C
  3. Activated protein C + cofactor protein S down-regulates thrombin generation by degrading Va and VIIa
23
Q

Describe the termination and localisation of coagulation

A

Antithrombin binds to heparin on the surface of the vessel and binds to free thrombin

24
Q

What is fibrinolysis

A

The fibrinolytic system is activated by formation of fibrin

Generates plasmin to breakdown the fibrin clot

25
Q

Explain the process of fibrinolysis

A
  1. Fibrin formation
  2. Tissue plasminogen activator converts plasminogen to active plasmin
  3. Plasmin starts to break down fibrin
  4. Fibrin degradation products formed
  5. Antiplasmin prevents over activation and degradation
26
Q

What is thrombosis and what are the causes

A

Coagulation inhibitory mechanism where there is an inappropriate clot formation
antithrombin deficiency
Protein C deficiency
Protein S deficiency C

27
Q

What are the haemostatic mechanisms during bleeding

A

Coagulation factors and platelets decrease

Fibrinolytic factors and anticoagulant proteins increase

28
Q

Give the 4 stages of haemostasis plug formation

A

Vessel constriction
Formation of an unstable platelet
Stabilisation of the plug with fibrin
Vessel repair and dissolution of the clot

29
Q

Explain the process of adhesion and aggregation

A 
Platelet adhesion via GIpIb 
Platelet aggregation 
1. Change in shape 
2. Release of Ca2+ from the stores
3. ADP release from the dense granule, vWF from the alpha granule
4. Thromboxane release
5. Expression of GPIIb or IIIa 
6. aggregation via GPIIb and fibrinogen
30
Q

Give an example of what causes deficiency or defect in collagen in the vessel wall

A

Steroid therapy
Age
Scurvy

31
Q

Give an example of what causes deficiency or defect of Von willebrand factor

A

Von Willebrand disease
type 1 - Not enough
Type 2 - incorrect vWF
type 3 - none produced

32
Q

Give an example of what causes deficiency or defect of platelets

A

Aspirin and other drugs

Thrombocytopenia

33
Q

Describe primary haemostatic bleeding

A

Bleeding is not delayed
May arise from defect or deficiency of collagen, VWF or platelets
Many congenital and acquired causes
Petechiae are typical of thrombocytopenia

34
Q

What is abnormal bleeding is characterised by

A

bleeding being spontaneous, prolonged or out of proportion to the injury

35
Q

What is the pattern of bleeding primary haemostasis fails due to VWF

A 
platelets cannot bind to VWF, do not slow down and cannot bind to collagen
Immediate
Easy bruising
Nosebleeds
Gum bleeding
Menorrhagia
Bleeding after trauma/surgery 
Petechiae (thrombocytopenia)
36
Q

Give some causes of secondary haemostasis disorders

A 
Defects of coagulation
Genetic: 
Haemophilia 
Protein C or S deficiency 
Antithrombin deficiency 
Factor 5 Leiden
Acquired:
Liver disease
Drugs 
Dilution 
Consumption
37
Q

Give the pattern of bleeding for defects in secondary haemostasis

A 
Often delayed and prolonged
Deeper, seen in joints and muscles
Not from small cuts
Nosebleeds are rare
Bleeding after trauma or surgery
After injections
38
Q

How do defects of coagulation come about

A

Deficiency or defect of coagulation factors which results in inadequate thrombin generation

39
Q

Describe haemophilia

A

Not enough FVIII (A) or FIX (B)
Coagulation does not occur
Hereditary
Failure to generate fibrin to stabilise the platelet plug
Spontaneous haemarthrosis is the hallmark of haemophilia (swollen, very painful)
Making a small cut will stop bleeding in 10 minutes

40
Q

Describe disseminated intravascular coagulation

A

Tissue factors are expressed on the inner surface of the blood vessels
Leads to activation of coagulation, consuming and depleting coagulation factors and platelets
Activation of fibrinolysis depletes fibrinogen

Associated with sepsis, major tissue damage, inflammation
Widespread bleeding, from IV lines, bruising, internal
Deposition of fibrin causes organ failure

41
Q

What proportions of deaths are caused by thombosis

A

10%

42
Q

What can thrombosis in arteries and veins cause

A

Artery - myocardial infarction, stroke, limb ischaemia

Vein - Pain and swelling

43
Q

What can embolism in the arteries and veins cause

A 
Arterial emboli (usually the heart) - may cause stroke or limb ischaemia
Venous emboli (lungs) - pulmonary embolus
44
Q

What are the risk factors for thrombosis

A 
Breaking bones/ fracture
Age
Pregnancy
Cancer
thrombosis at a young age
AT deficiency
45
Q

What is Virchow’s triad

A

Helps classifies the factors that cause thrombosis
Vessel wall - Endothelial injury
Flow - Stasis (in the venous circulation) or turbulent blood flow (causes PEs)
Blood - Blood hypercoagulability - genetic or acquired

46
Q

Explain how the vessel wall affects thrombosis risk

A

expression of proteins required for coagulation is altered during inflammation e.g. malignancy, infection, immune disorders

47
Q

Explain how blood affects thrombosis risk

A

Deficiency of anticoagulant proteins: Antithrombin, protein C, protein S
increase in coagulant proteins

48
Q

Describe the therapy for thrombosis

A

Restore the balance of haemostasis
Lyse the clot e.g. tPA
Limit recurrence/ emboli by:
Heparin - increasing anticoagulant activity
Warfarin - lower procoagulant factors
Rivaroxaban, apixaban - inhibit procoagulant factors

49
Q

How does the contraceptive pill affect haemostasis

A

The oestrogen in the combined contraceptive pill affects several coagulation proteins, most notably increasing factors VIII, X and XII. It reduced protein S (which has anticoagulant properties) and there is a general reduction in fibrinolytic activity. This is also seen in pregnancy.

50
Q

What is heparin used for

A

Immediate anticoagulation in venous thrombosis and pulmonary embolism
Works with antithrombin to inhibit thrombin

51
Q

Describe the acquired causes of secondary haemostasis disorders

A

Liver disease - Less liver synthesis so less coagulation factors produced
Drugs - Heparin (antithrombin) and warfarin (II, VII, IX, X synthesis inhibition) causes bleeding
Dilution - Lower concentration of coagulation factors
Consumption - Disseminated intravascular coagulation

52
Q

Describe the genetic causes of secondary haemostasis disorders

A

Haemophilia
Antithrombin deficiency - no IIa breakdown
Protein C/S deficiency - no FV and FVIII breakdown
Factor 5 Leiden - polymorphism, resistant to breakdown by protein C

53
Q

What are some fibrinolytic disorders

A 
Genetic: 
antiplasmin deficiency (-)

Acquired (+):
Excessive administration of plasmin/tPA
Tumour secreting plasmin

Cardiovascular System (13 decks)

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