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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
What are the 2 forms of heparin
Unfractioned | Low molecular weight - LMWH
26
How do you monitor heparin therapy
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
What are the potential complications of heparin therapy
Bleeding Heparin induced thrombocytopaenia - need to monitor FBC Osteoporosis - long term use
28
How can you reverse the action of heparin
Stop the drug - short half life | If the bleeding is severe then give protamine sulphate
29
How does warfarin work
It antagonises vitamin K This is required for final carboxylation of factors 2,7,9 and 10 Without it they cannot bind properly
30
What class of anticoagulant is warfarin
Coumarin anticoagulants | Other examples include - phenidione
31
How is vitamin K absorbed
Fat soluble vitamin Absorbed upper intestine Requires bile salts for absorption
32
How do you monitor warfarin therapy
INR | This is a standardised report of PT
33
Why does warfarin need to be carefully monitored
Narrow therapeutic window
34
Warfarin needs to be taken at the same time each day - true or false
TRUE
35
How is warfarin therapy established
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
How do you calculate the INR
Patients PT in seconds over the mean normal PT in seconds | All to the power of the International Sensitivity Index
37
What is the major adverse effect of warfarin therapy
Haemorrhage risk Can be mild such as nosebleeds and bruising Can be severe = GI, intracerebral
38
Which factors can influence bleeding risk in warfarin therapy
Intensity of anticoagulation Concomitant clinical disorders Concomitant use of other medications
39
How do you reverse the action of warfarin
Stop the warfarin Administer oral Vitamin K - takes about 6 hours to work Administer clotting factors (factor concentrates) - work immediately
40
How does dabigatran work
It inhibits thrombin | Its a new anticoagulant
41
Give examples of factor Xa inhibitors
Rivaroxaban | Edoxaban
42
How are the new anticoagulants administered
Orally | They do not require monitoring
43
Describe the process of atherosclerosis
Damage to endothelium Recruitment of ‘foamy’ macrophages rich in cholesterol Forms plaques rich in cholesterol
44
Describe the structure of stable atherosclerotic plaques
Hyalinised and calcified
45
Stable atherosclerotic plaques are seen in which diseases
``` Stable angina (coronary artery) Intermittent claudication (leg artery) ```
46
Unstable atherosclerotic plaques are seen in which diseases
Unstable angina or myocardial infarction (coronary arteries) Stroke (cerebral arteries) Will have a sudden onset of symptoms
47
List risk factors for arterial thrombosis
``` Hypertension (damage to endothelium, platelet activation) Smoking (endothelium, platelets) High cholesterol (accumulated in plaque) Diabetes mellitus (endothelium, platelets, cholesterol) ```
48
How can you prevent arterial thrombosis
``` Stop smoking Treat hypertension Treat diabetes Lower cholesterol Anti-platelet drugs ```
49
How do platelets adhere to subendothelial collagen
Via Glycoprotein 1b and Von Willebrand Factor.
50
List some of the molecules that platelets secrete to lead to aggregation
ADP | Thromboxane A2
51
How does aspirin work
Inhibits cyclo-oxygenase which is necessary to produce Thromboxane A2 This reduces platelet aggregation as thromboxane A2 is usually released from activated platelets
52
What are some of the side effects of aspirin
Bleeding | GI ulceration Bronchospasm as a result of prostaglandin production being blocked
53
How do clopidogrel and prasugrel work
They are ADP receptor antagonists | Work as anti-platelets
54
How does dipyridamole work
Phosphodiesterase inhibitor -reduces production of cAMP which is a ‘second messenger’ in platelet activation
55
How do GP IIb/IIIa inhibitors work
Antiplatelets | They inhibit aggregation as platelets attach to each other via GPIIbIIIa
56
Give an example of a GP IIb/IIIa inhibitors
Abciximab
57
How can you reverse the effects of anti-platelets
If serious bleeding - can reverse with platelet transfusion
58
How do you diagnose a DVT
D-dimers – may be raised Doppler US of leg If US is inconclusive then you can do a venogram
59
How do you treat a DVT
Immediate treatment of the DVT 6 months of anti-coagulation Follow up in clinic 1 month after Come off the OCP if combined
60
How can you reduce the risk of thrombosis
``` Prophylaxis – anticoagulants such as LMWH Compression stockings Flowtron boots Elevation of legs Early mobilisation ```
61
What tests constitute a coagulation screen?
Platelet count, PTT and APTT, fibrinogen
62
Which anti-coagulant is better for acute treatment
Heparin - fast acting | Warfarin takes a while to build up
63
When would you measure D-dimers
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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