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Haematology Year 3 > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

two types of thombotic events

A

arterial
- coronary, cerebral, peripheral

venous
- DVT/PE

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2
Q

Differences between arterial + venous systems

A

arterial
- much thicker, have to withstand higher pressures

venous
- thinner, lower pressure, have valves

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3
Q

what causes an arterial thrombosis

A

atherosclerosis

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4
Q

how is an arterial thrombosis formed

A

damage to the epithelium – platelets adhesion + aggregation – coagulation – may completely occlude the vessel or can embolise

platelet rich thrombus

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5
Q

treatment of arterial thrombus

A

aspirin / clopidogrel

modify risk factors for atherosclerosis

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6
Q

what is activated in a venous thrombosis

A

coagulation cascade i.e. fibrin clot

platelets not activated

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7
Q

what dysfunction leads to venous thrombosis

A

dysfunction in VIRCHOW’S TRIAD

  • stasis
  • vessel wall damage
  • hypercoagulability
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8
Q

treatment of venous thrombosis

A

heparin/warfarin/ other new oral anticoagulants

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9
Q

which type of thrombus is platelet rich

A

arterial

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10
Q

which type of thrombus is fibrin rich

A

venous

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11
Q

signs of DVT

A

limb feels HOT, SWOLLEN, TENDER

pitting oedema

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12
Q

signs of PE

A

pleuritic chest pain
hypoxia
cardiovascular collapse
right heart strain

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13
Q

risk factors for venous thromboembolism

A 
Age 
obesity
pregnancy 
previous DVT/PE
trauma/surgery 
oestrogen therapy 
thrombophilia 
paralysis
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14
Q

why is pregnancy a risk factor for venous thromboembolism

A

clotting factors raise to about 3 times normal level to prepare for child birth

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15
Q

why does hypercoagulability increase risk of venous thromboembolism

A

all associated with the release of tissue factor, raised VWF and factor 8

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16
Q

what is thrombophilia

A

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

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17
Q

mechanism for thrombophilia

A

decreased anti-coagulant activity

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18
Q

potential reasons for decreased anti-coagulant activity in thrombophilia

A

low levels of antithrombin III

low levels of protein C and S

19
Q

role of protein C and S

A

switch off factor V, VIII, X

20
Q

most common cause for decreased anti-coagulant activity

A

Factor V leiden

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

21
Q

what are hereditary thrombophilias

A

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

22
Q

examples of hereditary thrombophilias

A 
factor V leiden 
prothrombin 20210 mutation 
anti-thrombin deficiency 
protein C deficiency 
protein S deficiency
23
Q

when should hereditary thrombophilia screening be considered

A 
venous thrombosis <45 years old
recurrent venous thrombosis 
unusual venous thrombosis 
family history of venous thrombosis 
family history of thrombophilia
24
Q

management of hereditary thrombophilia

A

advice on avoiding risk
short term prophylaxis
- to prevent thrombic events during periods of known risk e.g. long haul flight

short term anticoagulation
- to treat thrombotic events

long term anticoagulation
- if recurrent thrombotic events

25
Q

what is a risk of long term anticoagulation

A

serious haemorrhage

26
Q

what is the most important tool in assessing risk of recurrent thrombosis

A

clinical history

  • history of previous thrombosis
  • spontaneous thrombosis
  • family history
27
Q

example of an acquired thrombophilia

A

antiphospholipid syndrome

28
Q

which has a higher risk of thrombosis - anti-phospholipid or hereditary thrombophilia

A

anti-phospholipid syndrome

29
Q

features of antiphospholipid syndrome

A 
young women
recurrent thromboses - DVT, PE
recurrent fetal loss
mild thrombocytopenia 
other autoimmune conditions
30
Q

antibodies seen in antiphospholipid syndrome

A

anti-cardiolipin

lupus anticoagulant

31
Q

effects of antibodies in antiphospholipid syndrome

A

conformation change in beta2 glycoprotein 1

- activation of primary + secondary haemostasis + vessel wall abnormalities

32
Q

treatment of anti-phospholipid

A

aspirin + warfarin

  • both given as there is activation of primary and secondary haemostasis systems – risk of arterial + venous thrombosis
33
Q

how does atherosclerosis occur

A
  • damage to endothelium
  • recruitment of foamy macrophage rich in cholesterol
  • forms plaques rich in cholesterol
  • calcifies – hardens arteries
34
Q

how do stable atherosclerotic plaques present

A

intermittent symptoms on exertion
e.g. angina (coronary artery)
claudication (leg artery)

35
Q

what happens when an unstable plaque ruptures

A

plaque ruptures – platelets are recruited + cause acute thrombosis

sudden onset of symptoms
e.g. central crushing chest pain, SOB in MI

36
Q

arterial thrombosis risk factors

A

hypertension
smoking
high cholesterol
diabetes

37
Q

what chemicals released by platelets enhance platelet recruitment to the site

A

ADP

thromboxane A2

38
Q

How does clopidogrel work

A

ADP receptor antagonist

39
Q

how does aspirin work

A

inhibits COX1 – this is necessary to produce thromboxane A2

40
Q

side effects of aspirin

A
  1. bleeding

2. blocks prostaglandin production – GI ulceration/bronchospasm

41
Q

DVT prophylaxis

A

TED stockings
physio
early mobilisation
heparin/warfarin

42
Q

how does dipyridamole work

A

phosphodiesterase inhibitor- decreases production of cAMP

43
Q

tamoxifen

A

increases DVT risk

Haematology Year 3 (21 decks)

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