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
what are risk factors for arterial thrombosis
Hypertension [damage to endothelium > platelet activation] Smoking High cholesterol Diabetes
26
how is an arterial thrombosis prevented
``` Stop smoking Treat hypertension Treat diabetes Lower cholesterol Anti-platelet drugs ```
27
what chemicals do platelets secrete to recruit more platelets to the site i.e. activation
ADP | Thromboxane A2
28
how do platelets bind to sub endothelial collagen i.e. adhesion
Glycoprotein 1b and Von Willebrand Factor.
29
how to platelets attach to each i.e. aggregation
via fibrinogen and GPIIbIIIa
30
how does aspirin work
Inhibits cyclo-oxygenase [COX 1] which is necessary to produce Thromboxane A2
31
what are side effects of aspirin
1. Bleeding 2. Blocks production of prostaglandins: - GI ulceration - Bronchospasm
32
how does Clopidogrel and prasugrel work
ADP receptor antagonists
33
how does dipyridamole work
Phosphodiesterase inhibitor -reduces production of cAMP which is a ‘second messenger’ in platelet activation
34
how does abciximab work
GP IIb/IIIa inhibitors | - inhibit aggregation
35
how can serious bleeding in anti platelet therapy be reversed
platelet transfusion
36
what must happen prior to surgery is someone is on anti platelet therapy
stop anti-platelet agents 7 days prior
37
Sx and Signs of DVT
Unilateral Pain Swelling Erythema
38
Sx and signs of PE
SOB Pleuritic chest pain Rub Hypoxia
39
what is DVT prophylaxis and Tx
TED stockings Physiotherapy Early mobilisation Heparin Warfarin