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Blood > Haemostasis 5 > Flashcards

Haemostasis 5 Flashcards

1
Q

What is a thrombus?

A

A solid mass in a blood vessel or heart

Process is called thrombosis

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2
Q

What makes up a thrombus?

A

Variable amounts of platelets, fibrin, trapped red cells

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3
Q

What is Virchow’s Triad and how does it relate to thrombosis?

A

Abnormal blood flow
Endothelial damage
Hypercoagubility

  • varying combinations of these 3 factors cause thrombosis
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4
Q

How does endothelial injury contribute to thrombosis?

A

Exposes vWF, collagen, tissue factor

Permits platelet adhesion

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5
Q

How does altered blood flow contribute to thrombosis?

A

Veins: stasis - accumulation of activated coagulation factors and activated platelets
Arteries: activation of platelets and vWF = activated by turbulent flow/high shearing stress

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6
Q

How does Hypercoagubility contribute to thrombosis?

A

Veins - increased concentration of coagulation factors or reduced functional levels of coagulation inhibitors
Arteries - some autoantibodies may trigger thrombosis

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7
Q

What are common causes for endothelial injury?

A

Endocardial injury - following MI, heart valve disease
Arterial injury - ulcerated/ruptured atherosclerotic plaque, agents toxic to endothelium, haemodynamic stress
Inflammation affecting blood vessels - vasculitis, trauma

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8
Q

When does a mural thrombus often form and why?

A

Mural thrombus on the endocardium after an MI.

  • Endothelium survives, but is injured by products from ischaemic and necrotic underlying muscle.
  • Stasis occurs between inactive trabeculae
  • Patients with MI have risk factors for increased coagulability
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9
Q

Describe how loss of laminar flow in arteries contributes to thrombosis.

A

High flow rates result in turbulence.
Causes endothelial injury through shearing stresses and activation of adhesion receptors.
Platelet activation
Activated platelet impact on and adhesion to endothelium.

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10
Q

Which arteries are sites of turbulence and are at risk of atherosclerosis and mural thrombosis?

A

Aorta and branches

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11
Q

When does stasis in veins occur?

A

During surgery and in patients lying still

Pressure on calf muscles, lack of movement

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12
Q

What issues surround stasis in veins?

A

Low flow or intermittent flow or no flow
Endothelial cell activation is promoted - platelets adhere
More platelets contact the vessel wall if blood is not flowing

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13
Q

How does surgery and trauma relate to stasis of the veins in the LL?

A

Activated coagulation factors and platelets in circulation
- Not washed away and dilluted by blood flow
-Not inactivated if concentration increases too rapidly
Small thromboses form
- may propagate (extend/grow)
- may undergo fibrinolysis

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14
Q

Describe how the development of a venous thrombus occurs.

A

Dynamic process over time.

  • Blood must flow past developing thrombus for platelets and fibrin activation to propagate (extend) the thrombus
  • Does not adhere well to wall
  • Fragments may break off and form a thrombotic embolus

Thrombus attached firmly at injury site

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15
Q

What is hypercoaguability?

A

Any alteration of coagulation pathways increases the risk for thrombosis
Often multifactorial
- genetic or acquired
- increased concentration of coagulation proteins
- decreased concentration of coagulation inhibitors
- most common factor: inflammation

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16
Q

Name the consequences of thrombosis.

A

Arterial thrombosis - ischaemia and infarction

17
Q

Describe how thrombosis in a diseased artery occurs.

A

Usual predisposing factor is rupture of an atherosclerotic plaque. This triggers platelet aggregation, fibrin formation and extension of thrombus to occlude vessel.

18
Q

What is the consequence of venous thrombosis?

A

Pulmonary embolus - thrombotic embolus lodged in pulmonary artery

19
Q

What are acute consequences of venous thrombosis?

A

Local pain and oedema (swelling)
Valves often lost from veins
Pulmonary embolism

20
Q

What are chronic consequences of venous thrombosis?

A 
Raised pressure in veins 
Varicose veins 
Chronic ulcers at ankle after minimal trauma 
Chronic pain in leg
Swelling
21
Q

What happens in varicose veins?

A

Vein diameter increases and vein elongates under sustained pressure due to incompetent valves

22
Q

What are further consequences of venous thrombosis?

A

Recurrent thrombosis

Recurrent pulmonary embolism

23
Q

What is thrombophilia?

A

Increased risk for thrombosis

  • acquired or genetic
  • arterial or venous
  • may be multifactorial
24
Q

What are common risk factors for arterial thrombosis?

A 
Hyperlipidaemia 
HTN 
Diabetes
Cigarette smoking 
Male 
Family Hx 
Polycythaemia 
Elevated fibrinogen 
Homocysteine
25
Q

Name factors causing other acquired thrombophilias - arterial or venous thrombosis.

A

Raised coagulation factor concentration or reduced inhibitor concentration
Antibodies that enhance platelet activation
Raised homocysteine
Loss of antithrombin in urine - low blood levels

26
Q

What causes an increased risk for thrombosis in women?

A

Oral contraceptive pill

27
Q

What is an acquired thrombophilia syndrome caused by an antibody?

A

Antiphospholipid syndrome

28
Q

What may antiphospholipid antibodies cause?

A

Venous/arterial thrombosis
Recurrent second trimester miscarriage
Thrombocytopenia

** Thrombosis + thrombocytopenia are important diagnostic clues that an antiphospholipid antibody may be present***

29
Q

Describe the pathogenesis of thrombosis in antiphospholipid syndromes.

A

Platelet activation
- turbulent blood flow or small amounts of thrombin

Autoantibody completes platelet activation resulting in thromboses and thrombocytopenia

30
Q

What does UF Heparin do?

A

Binds to antithrombin and increases activity

Immediate anticoagulation effect

31
Q

What does Low Molecular Weight Heparin do (LMWH)? And what is it used for?

A

Longer half life - once or twice daily dosing
Low dose - venous thromboprophylaxis in hospitals
High dose - full anticoagulation - injected medicine

Blood (8 decks)

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