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Haematology > Venous Thrombosis > Flashcards

Venous Thrombosis Flashcards

1
Q

what are common arterial thrombotic events

A

coronary- MI
cerebral- CVA
peripheral- pain, gangrene, loss of limb

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2
Q

what are common venous thrombotic events

A

DVT- lower limb most common

PE

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3
Q

what side of heart to DVTs go to when dislodged and cause a PE

A

right side

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4
Q

what moves blood in leg veins back to hearts

A

leg muscles and valves

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5
Q

what causes arterial thrombosis

A

athersclerosis- cholesterol plaque builds up
high pressure system causes plaque to rupture damaging vessel
this exposes collagen and causes platelet binding
platelet rich thrombus blocks vessel

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6
Q

what type of thombus is arterial

A

platelet rich

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7
Q

what is the treatment for arterial thrombosis

A

aspirin / other antiplatelet

modify risk factors for athersclerosis

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8
Q

what causes a venous thrombosis

A

low pressure system
virchows triad:
-stasis of blood: congeals
activates coagulation cascade- fibrin rich clot

  • vessel wall: deterioration of valves (age, previous VTE)
  • hypercoagulability (elevated tissue factor/ CF or low levels of antithrombin / proteins C and S)
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9
Q

what type of clot in venous thrombosis

A

fibrin rich

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10
Q

what type of drug for venous thrombosis

A

heparin/warfarin/ NOAC as secondary haemostasis

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11
Q

what is the biggest risk factor for VTE

A

previous VTE

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12
Q

what are the features of a DVT

A

limb feels hot, swollen and tender

pitting oedema

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13
Q

what are the differentials for a DVT

A

cardiac failure (would affect both legs)
infection
cellulitis

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14
Q

what are the consequences of PE

A 
(pulmonary embolism causing infarction) 
pleuritic chest pain (lodges peripherally, inflamed lung rubs on chest wall) 
cardiovascular collaspe/ death 
hypoxia 
right side heart strain (on ECG S1Q3T3)
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15
Q

what is the lifetime risk of a VTE

A

2.5%

highest when eldery/ pregnant/ post natal

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16
Q

what are the risk factors for VTE IN EXAMS

A

(anything that causes stasis, vessel wall damage or hypercoagulability)

age
marked obesity 
pregnancy 
puerperium 
oestrogen therapy 
previous DVT/ PE 
trauma/ surgery 
malignancy 
paralysis 
infection 
thrombophilia
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17
Q

what can cause stasis

A

age
obesity
pregnancy (gravid uterus can compress on veins)
previous DVT/PE
trauma/ surgery (esp lower limb orthopaedic)
malignancy
paralysis

18
Q

what are the common causes of vessel wall damage

A

age

previous DVT/PE

19
Q

what causes hypercoagulabilty

A 
anything that causes infection of inflammation: 
age
pregnancy and puerperium (oestrogen and CF 8 rise physiologically to prevent harmorrhage)
osterogen therapy
trauma/ surgery 
malignancy 
infection 
thrombophilia
20
Q

what component of haemostasis is a VTE usually caused by

A

failure of anticoagulant defences

21
Q

hypercoagulability causes the release and increase of what factors

A

release of tissue factor
raised VWF and CF 8
fibrinogen and other CF also activated

22
Q

what is thrombophilia

A

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

23
Q

what are the potential mechanisms of thrombophilia

A

decreased anticoagulant activity (most common)

increased coagulation (platelet plug/ fibrin clot formation)

decreased fibrinolytic activity

24
Q

what does the bodys anticoagulant activity do

A

switches off 2nd haemostasis

25
Q

what are naturally occurring anticoagulants

A

serine protease inhibitors (anti-thrombin)

protein C and protein S (switch off CF 5 and 8)

26
Q

what is the most common inherited thrombophilia

A

factor 5 leiden

27
Q

what are hereditary thrombophilias

A

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

28
Q

what are the types of hereditary thrombophilia

A 
factor 5 leiden (5x risk) 
prothrombin 20210 (2x risk) 
antithrombin def 
protein C def 
protein S def
29
Q

when should you consider hereditary thrombophilia screening

A 
VTE <45 y/o
recurrent VTE 
unusual VTE (e.g. in upper limb) 
FHx of VTE 
FHx of thrombophilia
30
Q

what is the management of hereditary thrombophilia

A

advice on risk avoidance
short term prophylaxis (during periods of known risk)
short term anticoagulation (to treat thrombotic events)
long term anticoagulation (if recurrent thrombotic events)

31
Q

will everyone with hereditary thrombophilia have a thrombosis

A

most will never

lots of other influences e.g. RFs

32
Q

what do you need to consider in long term anticoagulation

A

risk of recurrent thrombosis
vs
risk of serious haemorrhage
(warfarin annual rate of ICH 1 in 200)

33
Q

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

A

history of previous thrombosis
spontaneous thrombosis rather than acquired transient risk factor (immobility/ surgery)

FHx
thrombophilia screen results

34
Q

name an acquired thrombophilia

A

antiphospholipid syndrome

35
Q

does hereditary thrombophilia or APS have a bigger risk for thrombosis

A

APS

36
Q

what is APS

A

autoimmune condition with antibodies against beta2 glycoprotein 1 which causes activation of primary and secondary haemostasis and vessel wall abnormalities

(get arterial- platelets- and venous- fibrin- clots)

37
Q

what are the features of APS

A

recurrent thrombosis:

  • arterial (common cause of TIA/ stroke in young)
  • venous

recurrent fetal loss (thrombosis in placenta)

mild thrombocytoenia (can have ITP like condition due to cross reactivity of antibody)

38
Q

what are the antiphospholipid antibodies

A

lupus anticoagulants

have specificity for anionic phsophlipids which prolong phosholipid dependent coagulation in vitro (APTT prolonged)

39
Q

what conditions are associated with antiphospholipid antbodies

A 
autoimmune disorders 
lymphoproliferative disorders (chronic lymphocytic leukaemia) 
viral infections (EBV)
drugs 
primary
40
Q

what is the treatment of APS

A

as activation of 1st and 2nd haemostasis get arterial and venous thrombosis so need aspirin (aterial) and warfarin (vein) (if given in pregnancy with APS drastically increase chance of live birth)

(warfarin preffered over NOACs as has some protection against arterial events too)

Haematology (27 decks)

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