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Haematology > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

How do you treat an arterial thrombosis

A

Aspirin and other anti-platelet drugs

Modify risk factors for atherosclerosis

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2
Q

How does an arterial thrombosis occur

A

Formation of atherosclerotic plaques - narrows the vessel and can cause hypoxia
In a high pressure system this has risk of rupture which then starts the clotting cascade
Clots can completely block of the vessel - MI etc

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3
Q

How does a venous thrombus occur

A

Stasis is the problem
The platelets aren’t activated as its a low pressure system so less risk of damage
Fibrin clots form due to hypercoagulability (more clotting factors)

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4
Q

What is Virchow’s triad

A

Stasis
Vessel wall issues
Hypercoagulability

increases risk of venous thrombosis

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5
Q

Arterial thrombi are rich in what

A

Platelets

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6
Q

Venous thrombi are rich in what

A

Fibrin

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7
Q

How do you treat venous thrombosis

A

Anti-coagulants

Heparin, Warfarin or the new oral anticoagulants

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8
Q

How does DVT present

A

Limb feels hot, swollen, tender.

Pitting oedema

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9
Q

What are the risk factors for venous thromboembolism

A 
Age
Marked obesity
Pregnancy
Puerperium
Oestrogen therapy
Previous DVT/PE
Trauma/Surgery
Malignancy
Paralysis/immobility
Infection
Thrombophilia
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10
Q

How does pregnancy affect clotting factors

A

Factor 8 levels rise x3 during pregnancy - hypercoagulable state
HRT or OCP tricks body into thinking its pregnancy (oestrogen) so CF raise with these too

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11
Q

What is a thrombophilia

A

Familial or acquired disorder of the haemostatic mechanism which are likely to predispose to thrombosis.
Most are due to a decrease in anticoagulant activity

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12
Q

How do hereditary thrombophilia’s present

A

Recurrent thromboses at a younger age than expected

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13
Q

List common hereditary thrombophilia’s

A 
Factor V Leiden - Protein C and S less effective at switching off factor 5
Prothrombin 20210 mutation
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
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14
Q

When should you consider screening someone for hereditary thrombophilia

A 
Venous thrombosis <45 years old
Recurrent venous thrombosis
Unusual venous thrombosis
Family history of venous thrombosis
Family history of thrombophilia
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15
Q

How do you manage hereditary thrombophilia

A

Advice on avoiding risk
Short term prophylaxis during periods of known risk
Short term anticoagulation to treat thrombotic events
Long term anticoagulation if recurrent thrombotic events

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16
Q

What factors from the history suggest a risk of recurrent thrombosis

A

Strongest risk = personal Hx of thrombosis
Spontaneous event - rather than brought on by surgery or immobility
Family history

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17
Q

What is antiphospholipid syndrome

A

Produce autoantibodies against a protein causing increased tendency for thrombosis
Activates both primary and secondary haemostasis

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18
Q

What are the features of antiphospholipid syndrome

A 
Recurrent thromboses
Arterial, including TIAs
Venous
Recurrent foetal loss
Mild thrombocytopenia
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19
Q

Why does antiphospholipid syndrome lead to miscarriage

A

Thrombosis in placenta prevents the baby from receiving what it needs to grow and survive
Will have recurrent miscarriage

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20
Q

What other conditions are associated with antiphospholipid antibodies (apart from anti-phospholipid syndrome)

A

Associated with other autoimmune disorders
EBV can act as a trigger
Lymphoproliferative Disorders
Drugs causing antibodies;

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21
Q

How do you treat anti-phospholipid syndrome

A

Treatment depends upon location of bloodclot
Arterial = antiplatelet (aspirin)
Venous = anticoagulant (warfarin)

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22
Q

What are the indications for anti-coagulants

A

Venous thrombosis

Atrial fibrillation

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23
Q

How is heparin administered

A

IV or SC

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24
Q

How does heparin work

A

Potentiates antithrombin - stabilises its complex with thrombin
Has an immediate effect

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25
Q

What are the 2 forms of heparin

A

Unfractioned

Low molecular weight - LMWH

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26
Q

How do you monitor heparin therapy

A

Activated partial thromboplastin time (APTT) for unfractionated

Anti-Xa assay for LMWH but usually no monitoring of LMWH is required as more predictable response

Also need to monitor FBC for thrombocytopaenia

27
Q

What are the potential complications of heparin therapy

A

Bleeding
Heparin induced thrombocytopaenia - need to monitor FBC
Osteoporosis - long term use

28
Q

How can you reverse the action of heparin

A

Stop the drug - short half life

If the bleeding is severe then give protamine sulphate

29
Q

How does warfarin work

A

It antagonises vitamin K
This is required for final carboxylation of factors 2,7,9 and 10
Without it they cannot bind properly

30
Q

What class of anticoagulant is warfarin

A

Coumarin anticoagulants

Other examples include - phenidione

31
Q

How is vitamin K absorbed

A

Fat soluble vitamin
Absorbed upper intestine
Requires bile salts for absorption

32
Q

How do you monitor warfarin therapy

A

INR

This is a standardised report of PT

33
Q

Why does warfarin need to be carefully monitored

A

Narrow therapeutic window

34
Q

Warfarin needs to be taken at the same time each day - true or false

A

TRUE

35
Q

How is warfarin therapy established

A

For acute thrombosis is can be given rapidly alongside heparin
Usually given slowly
Particularly for AF in community and for liver failure, malnourished, elderly

36
Q

How do you calculate the INR

A

Patients PT in seconds over the mean normal PT in seconds

All to the power of the International Sensitivity Index

37
Q

What is the major adverse effect of warfarin therapy

A

Haemorrhage risk
Can be mild such as nosebleeds and bruising
Can be severe = GI, intracerebral

38
Q

Which factors can influence bleeding risk in warfarin therapy

A

Intensity of anticoagulation
Concomitant clinical disorders
Concomitant use of other medications

39
Q

How do you reverse the action of warfarin

A

Stop the warfarin
Administer oral Vitamin K - takes about 6 hours to work
Administer clotting factors (factor concentrates) - work immediately

40
Q

How does dabigatran work

A

It inhibits thrombin

Its a new anticoagulant

41
Q

Give examples of factor Xa inhibitors

A

Rivaroxaban

Edoxaban

42
Q

How are the new anticoagulants administered

A

Orally

They do not require monitoring

43
Q

Describe the process of atherosclerosis

A

Damage to endothelium
Recruitment of ‘foamy’ macrophages rich in cholesterol
Forms plaques rich in cholesterol

44
Q

Describe the structure of stable atherosclerotic plaques

A

Hyalinised and calcified

45
Q

Stable atherosclerotic plaques are seen in which diseases

A 
Stable angina (coronary artery)
Intermittent claudication (leg artery)
46
Q

Unstable atherosclerotic plaques are seen in which diseases

A

Unstable angina or myocardial infarction (coronary arteries)
Stroke (cerebral arteries)

Will have a sudden onset of symptoms

47
Q

List risk factors for arterial thrombosis

A 
Hypertension (damage to endothelium, platelet activation)
Smoking (endothelium, platelets)
High cholesterol (accumulated in plaque)
Diabetes mellitus (endothelium, platelets, cholesterol)
48
Q

How can you prevent arterial thrombosis

A 
Stop smoking
Treat hypertension
Treat diabetes
Lower cholesterol
Anti-platelet drugs
49
Q

How do platelets adhere to subendothelial collagen

A

Via Glycoprotein 1b and Von Willebrand Factor.

50
Q

List some of the molecules that platelets secrete to lead to aggregation

A

ADP

Thromboxane A2

51
Q

How does aspirin work

A

Inhibits cyclo-oxygenase which is necessary to produce Thromboxane A2
This reduces platelet aggregation as thromboxane A2 is usually released from activated platelets

52
Q

What are some of the side effects of aspirin

A

Bleeding

GI ulceration
Bronchospasm
as a result of prostaglandin production being blocked

53
Q

How do clopidogrel and prasugrel work

A

They are ADP receptor antagonists

Work as anti-platelets

54
Q

How does dipyridamole work

A

Phosphodiesterase inhibitor -reduces production of cAMP which is a ‘second messenger’ in platelet activation

55
Q

How do GP IIb/IIIa inhibitors work

A

Antiplatelets

They inhibit aggregation as platelets attach to each other via GPIIbIIIa

56
Q

Give an example of a GP IIb/IIIa inhibitors

A

Abciximab

57
Q

How can you reverse the effects of anti-platelets

A

If serious bleeding - can reverse with platelet transfusion

58
Q

How do you diagnose a DVT

A

D-dimers – may be raised
Doppler US of leg
If US is inconclusive then you can do a venogram

59
Q

How do you treat a DVT

A

Immediate treatment of the DVT
6 months of anti-coagulation
Follow up in clinic 1 month after
Come off the OCP if combined

60
Q

How can you reduce the risk of thrombosis

A 
Prophylaxis – anticoagulants such as LMWH  
Compression stockings 
Flowtron boots
Elevation of legs 
Early mobilisation
61
Q

What tests constitute a coagulation screen?

A

Platelet count, PTT and APTT, fibrinogen

62
Q

Which anti-coagulant is better for acute treatment

A

Heparin - fast acting

Warfarin takes a while to build up

63
Q

When would you measure D-dimers

A

In patients deemed low risk of thrombosis by the clinical scoring system
In this cohort a negative result can safely exclude it

Haematology (8 decks)

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