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Thrombotic Disorders Flashcards

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1
Q

What is the difference between thrombosis and haemostasis?

A

Thrombosis is a blood clot forming INSIDE a blood vessel

Haemostasis is a blood clot forming on the surface of a blood vessel

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2
Q

What happens when blood cannot reach downstream tissues?

A

Leads to ischaemia

Death or dysfunction of tissues

Lack of blood leads to a shortage of oxygen and build up of toxins

Causes malfunction, pain and swelling of tissue

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3
Q

What are the two main types of venous thrombosis?

A

Deep vein thrombosis occurs in the arms or legs

Pulmonary embolism occurs in the lungs

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4
Q

What are the 4 main types of arterial thrombosis?

A

Myocardial infarction occurs in the heart

atrial fibrillation occurs in the heart

peripheral vascular disease occurs in the leg

stroke occurs in the brain

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5
Q

What is a deep vein thrombosis?

A

A blood clot that develops in a deep vein in the body

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6
Q

When and where does a DVT usually occur?

A

It occurs under low blood flow

The blood pools around the valves meaning the flow is unusual and the blood is static

It develops around the valves in the deep veins in the legs and arms

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7
Q

What are the characteristics of the thrombus in DVT?

A

It is rich in fibrin and erythrocytes

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8
Q

What does DVT cause?

A

Pain and swelling in the leg

Can lead to pulmonary embolism

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9
Q

How is a pulmonary embolism caused?

A

A part of the deep vein thrombus breaks off to form an embolus

The embolus travels via the vena cava, right atrium and right ventricle to the lung

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10
Q

What can pulmonary embolism lead to?

A

The embolus will block an artery in the lung and lead to lung infarction

It can persist for a long time and lead to post-thrombolytic syndrome

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11
Q

What are the common symptoms of post-thrombolytic syndrome?

A

Redness, swelling, ulcers and chronic leg pain

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12
Q

What are the symptoms of pulmonary embolism and why is it hard to diagnose?

A

Tiredness, chest pain, coughing up blood, struggle to breathe

Often misdiagnosed for a lung infection

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13
Q

What are the 5 risk factors for venous thrombosis?

A 
Immobilisation
surgery
cancer
oral contraceptives
genetic risk factors
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14
Q

Why is immobilisation a risk factor for DVT?

A

The blood is stagnant and not circulating enough

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15
Q

Why is surgery a risk factor for DVT?

A

Increased risk due to immobilisation after surgery

large release of TF into the blood after injury, leading to increased coagulation

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16
Q

Why is cancer a risk factor for DVT?

A

Cancer cells express TF

some TF may be inside the blood vessel

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17
Q

Why are oral contraceptives a risk factor for DVT?

A

The effects of the hormones on the coagulation system cause the blood to become more procoagulant

This occurs during pregnancy too

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18
Q

What are the genetic factors that increase risk of DVT?

A

Deficiency in coagulation inhibitors

Factor V Leiden mutation

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19
Q

What are the 3 main risk factors that contribute to thrombosis?

A

Stasis - pooling of blood

Endothelial dysfunction - endothelium becomes more procoagulant as there is more TF expression

Hypercoagulable state - the balance in the coagulation system is disrupted and the blood becomes more procoagulant

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20
Q

What does Virchow’s triad show?

A

The balance between the 3 categories of risk factors that contribute to thrombosis

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21
Q

What happens if the haemostatic balance is disrupted?

A

If there are more procoagulant mechanisms, this leads to thrombosis

if there are more anticoagulant mechanisms, this leads to bleeding

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22
Q

What is the role of coagulation inhibitors?

A

They prevent clotting

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23
Q

What is antithrombin?

What does it inhibit and what is its role?

A

It is a small protein produced by the liver

It binds to the active site of thrombin

It inhibits thrombin, FXa and FIXa

It regulates blood clot formation by slowing down the process and preventing excessive clotting

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24
Q

What is tissue factor pathway inhibitor?

What does it inhibit and what is its role?

A

It is a single chain polypeptide

It irreversibly inhibits FXa

When FXa is inhibited, the FXa-TFPI complex can inhibit the FVIIa-TF complex

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25
What is activated protein C? What does it inactivate?
It is a Vitamin K dependent enzyme and serine protease It proteolytically inactivates FVa and FVIIIa
26
How is protein C activated?
Protein C is an inactive zymogen It is activated when it binds to thrombin
27
What is the risk of an APC deficiency?
APC is an anticoagulant APC deficiency leads to increased risk of thrombosis
28
What is Protein S?
It is a cofactor for APC in the inactivation of FVa and FVIIIa
29
What is meant by 'idiopathic'?
There is no clear triggering factor for a condition
30
What is APC resistance?
APC does not stop the blood from clotting Leads to thrombosis
31
What is Factor V Leiden?
Inherited activated Protein C resistance Increases the risk of DVT
32
How is Factor V Leiden caused?
Point mutation in the Factor V gene Factor V is the substrate for APC
33
How does Factor V Leiden increase the risk of developing DVT in homozygotes and heterozygotes?
In heterozygotes, risk of developing a DVT is increased by 3 to 8 times In homozygotes, risk of developing a DVT is increased by 50 to 80 times
34
How does APC usually inactivate FVa?
It cleaves 3 peptide bonds in FVa to inactivate it FVa helps to make more thrombin unless it is inactivated by proteolytic cleavage
35
Why can't APC cleave FVa in Factor V Leiden? What is the consequence?
There is a mutation in one of the three APC cleavage sites Factor V Leiden is resistant to APC cleavage FVa is fully active leading to procoagulant activity
36
What is fibrinolysis?
The enzymatic breakdown of fibrin in blood clots
37
What must be activated in order for fibrinolysis to occur? Where is this found?
Plasminogen is a zymogen that is incorporated into the clot when it is formed It must be converted to plasmin Plasmin is an active serine protease
38
What are the 2 cofactors involved in converting plasminogen to plasmin?
Tissue plasminogen activator (t-PA) Urokinase (uPA)
39
How is t-PA released and how does this lead to fibrinolysis?
t-PA is released into the blood by the damaged endothelium of blood vessels Plasminogen trapped in the clot becomes slowly activated Plasmin begins to break down the fibrin mesh
40
What will inhibit t-PA and uPA?
plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 PAI-1 and PAI-2
41
What will inhibit plasmin?
Alpha 2-antiplasmin Alpha 2-macroglobulin
42
How does plasmin further stimulate plasmin generation?
It produces more active forms of tPA and urokinase
43
What are D-Dimers?
Part of the fibrin molecule that results from chopping up the fibrin fibres during fibrinolysis
44
What do the levels of D-dimer in the blood show?
Levels of D-dimer are much higher in thrombosis patients Increased clotting leads to increased degradation of clots If D-dimer levels are normal, there is NOT a pulmonary embolism
45
What is primary and secondary fibrinolysis?
Primary occurs naturally by the body Secondary occurs as a result of drug intervention
46
What are tPA and uPA used for clinically?
They are clot busting drugs Secondary fibrinolysis
47
What 2 treatments for venous thrombosis have an immediate onset of the anticoagulant effect?
Unfractionated heparin Intravenous and helps antithrombin to inhibit thrombin and FXa Low molecular weight heparin Small fragments given subcutaneously and have longer term effects
48
Why is low molecular weight heparin safer?
Heparin is purified from bovine intestines so there may be some impurities
49
What treatment for venous thrombosis has a slower onset of the anticoagulant effect?
Vitamin K Antagonists VKAs have a slower onset but longer term anticoagulation effect
50
What is Dabigatran?
A direct thrombin inhibitor used to treat venous thrombosis
51
What is the main cause of arterial thrombosis?
It is caused by atherosclerosis The thrombosis is triggered by the rupture of an atherosclerotic plaque
52
What are 2 life threatening events that result from arterial thrombosis?
Myocardial infarction (coronary artery) | Ischaemic stroke carotid artery
53
The risk factors for arterial thrombosis are the same as atherosclerosis and include...
``` advanced age smoking diabetes hypertension high cholesterol poor diet lack of exercise ```
54
How do monocytes begin the process of plaque formation?
Monocytes infiltrate under the endothelium to deal with inflammation They convert to macrophages Macrophages become foam cells as they begin to digest cholesterol Foam cells begin to die and express tissue factor
55
Where is the fibrous cap in a plaque and what is it made from?
Found below the endothelium Made from collagen and smooth muscle
56
What is found in the necrotic core of the plaque?
Cholesterol and debris of necrotic cells This is the atheroma
57
What 3 things within the plaque can activate platelets?
Collagen activates platelets via GPVI Lysophosphatidic acid (LPA) activates platelets via P2Y Tissue factor expressed by foam cells binds to FVII and activates coagulation
58
How does rupturing of the plaque leads to a clot?
When the plaque ruptures, there is a major procoagulant stimulus Exposure of the atheroma leads to a fibrin/platelet clot
59
What are antiplatelet drugs?
They decrease platelet aggregation and inhibit thrombus formation in arterial circulation Used to treat arterial thrombosis
60
How does aspirin work as an antiplatelet drug?
It inhibits COX-1 and thromboxane production
61
How do the antiplatelet drugs, Abciximab and Tirofiban, work?
They are anti aIIbB3 drugs They block the receptor for fibrinogen and von Willebrand factor
62
How do the antiplatelet drugs, Clopidogrel, Ticagrelor and Prasugrel, work?
They are anti P2Y drugs They block the receptor for ADP induced platelet aggregation
63
What are fibrinolytic drugs?
Clot-busting drugs They are derivatives of tPA and/or uPA
64
What treatments are used to prevent stroke in patients with atrial fibrillation?
VKAs such as Warfarin Direct thrombin inhibitors (Dabigatran, Melagratran, Argatroban) Direct anti-Xa drugs (Rivaroxaban, Apixaban)
65
What is the problem with using VKAs?
Close monitoring with INR
66
What is a problem with using anticoagulation drugs?
Increased risk of bleeding

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