Thombosis Flashcards

1
Q

what are the two types of thrombotic events

A

Arterial
- Coronary, cerebral, peripheral

Venous
- DVT or PE

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2
Q

how does the venous system and the arterial system differ

A

arterial system
- much thicker, much higher pressure system

venous
- thinner, lower pressure, valves, platelets don’t get activated

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3
Q

what causes an arterial thrombosis

A

Atherosclerosis - damage to the epithelium, cholesterol plaque, it rupture, platelets stick to it, can lead to occluding the vessel

Therefore, a Platelet rich thrombus

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4
Q

what is the Tx for an arterial thrombosis

A

Aspirin or Clopidogrel

Modify risk factors for atherosclerosis

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5
Q

what is activated in a venous thrombosis

A

coagulation cascade i.e. fibrin clot

platelets not activated

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6
Q

what dysfunction in what triad leads to a venous thrombosis

A

think Virchow’s triad

  • stasis
  • vessel wall
  • hypercoagulability
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7
Q

what is the Tx for a venous thrombosis

A

heparin/warfarin/
other new oral anticoagulants

going after secondary haemostasis

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8
Q

what are risk factors for a venous thromboembolism

A
Age
Obesity
Pregnancy 
Puerperium - the 6 weeks after child birth
Oestrogen therapy 
Previous DVT/PE
Trauma/surgery 
Malignancy 
Paralysis 
Thrombophilia
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9
Q

why is pregnancy a risk factor for venous thromboembolism

A

clotting factors raise to about 3 times normal to prepare for childbirth to try stop bleeding

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10
Q

Age, Pregnancy, Puerperium, Oestrogen therapy, Trauma/surgery, Malignancy and infection are associated with Hypercoagulability - why does this increase the risk of a venous thromboembolism

A

they are all associated with the release of tissue factor, raised vWF and factor 8.

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11
Q

what is thrombophilia

A

Familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis.

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12
Q

what are potential mechanisms for thrombophilia

A

increased coagulation activity
decreased fibrinolytic activity
decreased anti-coagulant activity

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13
Q

what are potential reasons for a decreased anti-coagulant activity

A

low levels of anti-thrombin III

low levels of protein C and S

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14
Q

what is the commonest cause for a decreased anti-coagulant activity

A

factor V leiden

- varient in factor V gene, makes it more difficult for protein C and S to switch it off

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15
Q

what are examples of HEREDITARY thrombophilia

A
Factor V Leiden
Prothrombin 20210 mutation
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
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16
Q

when should hereditary thombophilia screening be considered

A
Venous thrombosis <45 years old
Recurrent venous thrombosis
Unusual venous thrombosis
Family history of venous thrombosis
Family history of thrombophilia
17
Q

Mx of hereditary thombophilia

A

Advice on avoiding risk
Short term prophylaxis

Short term anticoagulation
- treat episodes

Long term anticoagulation
- if recurrent thrombotic events

18
Q

what is an example of an acquired thrombophilia

A

Antiphospholipid antibody syndrome

- more likely for thrombosis than hereditary thrombophilia

19
Q

what is features of Antiphospholipid antibody syndrome

A

young women, autoimmune presenting with CLOT

Clotting [DVT, PE]
Livedo reticularis
Obstetric (recurrent misarriages)
Thrombocytopenia (decreased platelets)

20
Q

what antibodies are seen in Antiphospholipid antibody syndrome

A

Anti-cardiolipin antibodies and lupus anti-coagulant.

21
Q

Tx of Antiphospholipid antibody syndrome

A

Aspirin and Warfarin

due to activation of both primary and secondary haemostasis&raquo_space; arterial and venous thrombosis

22
Q

how does atherosclerosis occur

A

Damage to endothelium

Recruitment of ‘foamy’ macrophages rich in cholesterol

Forms plaques rich in cholesterol

Hyalinised and calcified&raquo_space; arteries become hard

23
Q

what are stable Atherosclerotic plaques

A
stable angina (coronary artery), 
intermittent claudication (leg artery)
24
Q

what happens with an unstable Atherosclerotic plaque

A

Plaques rupture, platelets are recruited and cause acute thrombosis

Sudden onset of symptoms

Unstable angina or MI (coronary arteries)
Stroke (cerebral arteries)

25
Q

what are risk factors for arterial thrombosis

A

Hypertension [damage to endothelium > platelet activation]

Smoking

High cholesterol

Diabetes

26
Q

how is an arterial thrombosis prevented

A
Stop smoking
Treat hypertension
Treat diabetes
Lower cholesterol
Anti-platelet drugs
27
Q

what chemicals do platelets secrete to recruit more platelets to the site i.e. activation

A

ADP

Thromboxane A2

28
Q

how do platelets bind to sub endothelial collagen i.e. adhesion

A

Glycoprotein 1b and Von Willebrand Factor.

29
Q

how to platelets attach to each i.e. aggregation

A

via fibrinogen and GPIIbIIIa

30
Q

how does aspirin work

A

Inhibits cyclo-oxygenase [COX 1] which is necessary to produce Thromboxane A2

31
Q

what are side effects of aspirin

A
  1. Bleeding
  2. Blocks production of prostaglandins:
    - GI ulceration
    - Bronchospasm
32
Q

how does Clopidogrel and prasugrel work

A

ADP receptor antagonists

33
Q

how does dipyridamole work

A

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

34
Q

how does abciximab work

A

GP IIb/IIIa inhibitors

- inhibit aggregation

35
Q

how can serious bleeding in anti platelet therapy be reversed

A

platelet transfusion

36
Q

what must happen prior to surgery is someone is on anti platelet therapy

A

stop anti-platelet agents 7 days prior

37
Q

Sx and Signs of DVT

A

Unilateral
Pain
Swelling
Erythema

38
Q

Sx and signs of PE

A

SOB
Pleuritic chest pain
Rub
Hypoxia

39
Q

what is DVT prophylaxis and Tx

A

TED stockings
Physiotherapy
Early mobilisation

Heparin
Warfarin