Venous Thrombosis Flashcards

1
Q

types of arterial thrombotic events?

A

coronary
cerebral
peripheral

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2
Q

types of venous thrombotic events?

A

DVT

PE

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3
Q

artery vs vein?

A

artery has thicker muscle
artery actually pulsates itself
blood pumped through vein via contraction of surrounding muscles

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4
Q

what usually causes arterial thrombosis?

A

atherosclerosis leading to a platelet rich thrombus if plaque ruptures exposing collagen etc

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5
Q

treatment of arterial thrombosis?

A

aspirin and other anti-platelets

modify risk factors

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6
Q

what tends to be the problem causing venous thrombosis?

A
blood stasis (platelets not activated)
static blood tends to congeal and form a fibrin clot via the coagulation cascade
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7
Q

management of venous thrombosis?

A

target fibrin formation

warfarin, anticoagulants etc

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8
Q

virchows triad of cause of venous thrombosis?

A

venous stasis
damage to vessel wall (deterioration of valves due to age, previous clots etc)
hypercoagulable blood (elevated clotting factors due to illness or inherited low levels of naturally occurring anticoagulants such as protein C and S and antithrombin)

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9
Q

features of DVT?

A

limb feels hot, swollen and tender
pitting oedema
high WCC

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10
Q

signs of PE?

A
pleuritic chest pain
tachypnoea
tachycardia
hypoxia
cardiovascular collapse/death
right heart strain on ECG
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11
Q

risk factors for venous thromboembolism?

A
age (damaged vessels and lack of mobility)
obesity
pregnancy
puerperium(6 weeks following childbirth)
oestrogen therapy
previous DVT/PE (damages vessel wall)
trauma/surgery
malignancy
paralysis
infection
thrombophilia
anything that cause reduced mobility
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12
Q

stasis related risk factors?

A
age
obesity
pregnancy
previous DVT/PE
trauma/surgery
malignancy
paralysis
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13
Q

vessel wall related risk factors?

A

age

previous DVT/PE

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14
Q

hypercoagulability related risk factors?

A
age
pregnancy (increased CFs and oestrogen)
puerperium
oestrogen therapy (increases CFs)
trauma/surgery
malignancy
infection
thrombophilia
(increased TF, vWF and CF 8)
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15
Q

what part of haemostatic system tends to go wrong in thrombophilia?

A

anticoagulant defences

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16
Q

what is thrombophilia?

A

familial acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis

17
Q

potential mechanisms of thrombophilia?

A
decreased anticoagulant activity
increased coagulation (antiphospholipid syndrome)
18
Q

what are the naturally occurring anticoagulants which can be deficient in families?

A

anti-thrombin (type of serine protease inhibitor)

protein C and protein S (factor 5 leiden can reduce ability of protein C and S to switch off CF 5)

19
Q

what is hereditary thrombophilia?

A

group of genetic defects in which affected individuals have an increased tendency to develop premature unusual and recurrent thrombosis

20
Q

causes of hereditary thrombophilia?

A
presence of factor 5 leiden
prothrombin 20210 mutation
antithrombin deficiency
protein C deficiency
protein S deficiency
21
Q

when would a diagnosis of hereditary thrombophilia be considered?

A
venous thrombosis <45 years old
recurrent venous thrombosis
unusual venous thrombosis
family history of venous thrombosis
family history of thrombophilia
22
Q

management of hereditary thrombophilia?

A

advice to avoid risk
short term prophylaxis during periods of known risk
short term anticoagulation to treat thrombotic events
long term anticoagulation if recurrent thrombotic events

23
Q

when does a thrombotic event become likely in thrombophilia?

A

when there are multiple risk factors

often never have an event if no other risk factors are present

24
Q

risks of recurrent thrombosis in order of highest-lowest risk?

A

history of previous DVT/PE
spontaneous thrombosis rather than acquired risk factor (e.g immobility or surgery etc)
family history
thrombophilia screen results

25
Q

risk of thrombosis in antiphospholipid syndrome?

A

stronger risk factor than hereditary thrombophilia

26
Q

features of antiphospholipid syndrome?

A

recurrent arterial and venous thromboses (including TIA)
recurrent foetal loss
mild thrombocytopaenia

27
Q

pathogenesis of antiphospholipid syndrome?

A

antibodies lead to a conformational change in beta 2 glycoprotein 1 which leads to activation of both primary and secondary haemostasis and vessel wall abnormalities

28
Q

describe the antibodies in antiphospholipid syndrome

A

autoantibodies which have specificity for anionic phospholipids
also prolong phospholipid dependant coagulation tests in vitro (prolongs ATPP test even though there isn’t a clotting factor deficiency)
also known as lupus anticoagulants

29
Q

conditions associated with antiphospholipid antibodies?

A
autoimmune disorders
lymphoproliferative disorders
viral infection
drugs
primary
30
Q

management of antiphospholipid syndrome?

A

aspirin (venous thrombosis)

warfarin (arterial thrombosis)