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
what is a risk of long term anticoagulation
serious haemorrhage
26
what is the most important tool in assessing risk of recurrent thrombosis
clinical history - history of previous thrombosis - spontaneous thrombosis - family history
27
example of an acquired thrombophilia
antiphospholipid syndrome
28
which has a higher risk of thrombosis - anti-phospholipid or hereditary thrombophilia
anti-phospholipid syndrome
29
features of antiphospholipid syndrome
``` young women recurrent thromboses - DVT, PE recurrent fetal loss mild thrombocytopenia other autoimmune conditions ```
30
antibodies seen in antiphospholipid syndrome
anti-cardiolipin | lupus anticoagulant
31
effects of antibodies in antiphospholipid syndrome
conformation change in beta2 glycoprotein 1 | - activation of primary + secondary haemostasis + vessel wall abnormalities
32
treatment of anti-phospholipid
aspirin + warfarin - both given as there is activation of primary and secondary haemostasis systems -- risk of arterial + venous thrombosis
33
how does atherosclerosis occur
- damage to endothelium - recruitment of foamy macrophage rich in cholesterol - forms plaques rich in cholesterol - calcifies -- hardens arteries
34
how do stable atherosclerotic plaques present
intermittent symptoms on exertion e.g. angina (coronary artery) claudication (leg artery)
35
what happens when an unstable plaque ruptures
plaque ruptures -- platelets are recruited + cause acute thrombosis sudden onset of symptoms e.g. central crushing chest pain, SOB in MI
36
arterial thrombosis risk factors
hypertension smoking high cholesterol diabetes
37
what chemicals released by platelets enhance platelet recruitment to the site
ADP | thromboxane A2
38
How does clopidogrel work
ADP receptor antagonist
39
how does aspirin work
inhibits COX1 -- this is necessary to produce thromboxane A2
40
side effects of aspirin
1. bleeding | 2. blocks prostaglandin production -- GI ulceration/bronchospasm
41
DVT prophylaxis
TED stockings physio early mobilisation heparin/warfarin
42
how does dipyridamole work
phosphodiesterase inhibitor- decreases production of cAMP
43
tamoxifen
increases DVT risk