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Flashcards in Thrombosis and risk factors of thrombosis Deck (36):
1

what is virchows triad

blood flow, composition of blood and vascular endothelial.

2

what is the primary cause of a arterial thrombosis

atherosclerosis.

3

what is the pathogenesis of a arterial thrombosis

rupture of a atheromatous plaque
endothelial injury
platelet aggregation and platelet thrombi.

4

risk factors for arterial thrombi formation

smoking, hypertension, hypercholesterolaemia, diabetes, family history, obesity, physical inactivity, male and sex.

5

what is the main component of a venous thrombus

fibrin

6

what is the pathogenesis of venous thrombosis

venous stasis
hypercoagubale states.

7

symptoms of DVT

swollen, red, hot to touch, painful, unilateral leg

8

what secondary condition is DVT above the leg likely to present with

Pulmonary embolism

9

symptoms of PE

chest pain, breathlessness and haemotypysis.

10

how can hospital acquired VTE be prevented

risk assessment
prophyalaxis- “Low dose” low molecular weight heparin, fondaparinux
Newer anticoagulants- direct inhibitors of Factor Xa: rivaroxaban, direct thrombin inhibitors : dabigatran

11

how is hospital acquired VTE treated

care pathway- anticoagulant drugs.
If patient is at increased risk of bleeding provide stocking to improve circulation to the legs

12

what are the risk factors of VTE

• Active cancer or cancer treatment
• Age over 60 years
• Critical care admission
• Dehydration
• Known thrombophilias
• One or more significant medical comorbidities
• Surgery
• Major Trauma
• Personal history of VTE
• Use of hormone replacement therapy
• Use of oestrogen-containing contraceptive therapy
• Varicose veins with phlebitis
• Obesity (BMI over 30 kg/m2 )
• Pregnancy and postnatal period
• Immobility
• First degree relative with VTE

13

what molecules does unfractionated heparin work on.

anti thrombin (2 sites) and anti Xa

14

what molecule does LMW heparin bind

anti Xa, and anti thrombin
Factor Xa inhibitor

15

what molecule does Fondaparinux find to

anti Xa

16

what molecule do direct thrombin inhibitors act on

thrombin

17

What does a d-dimer test show

D-dimer breakdown product form fibrin clot.
Indicates that a clot was previously present although it has now been broken down

18

how can a ultrasound help diagnose a thrombus

Look for loss of flow signal, intravascular defects or non collapsing vessels in the venous system.
Vessels with clot will not compress if you apply pressure with the ultrasound probe.

19

what is a spiral/multi sliced CT used for

detect PE

20

what is a VQ scan

radio isotope scan.
Compare radioisotope pattern of a inhaled isotope (ventilation scan), injected isotope (perfusion scan)- this is diagnostic of DVT.

21

treatment plan for a uncomplicated patient with dot

Suspected DVT- single dose LMWH
confirm diagnosis-LMWH for 5 days.
Start warfarin
Start patient-held anti-coagulant book + inpatient warfarin chart

22

which anticoagulants are used as both treatment and prevention of DVT

• Rivaroxaban, Apixaban- direct factor Xa inhibitor
• Dabigatran- diresct thrombin inhibitor.-oral.
• Fondaparinux, LMWH- paraenteral

23

how long is DVT/VTE treated for upon first episode and what medication is typically used

3-6 months.
warfarin

24

what are recurrent episodes Recurrent episodes of VTE.

Treat with long term anticoagulation.
Recurrent episodes of VTE.

25

define thrombophillia

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

26

common inherited thrombophillias

• Antithrombin deficiciency
• Protein C deficiency
• Protein S deficiency
• Activated Protein C resistance/FV Leiden
• Dysfibrinogenaemia- give rise to bleeding, thrombosis or both.
• Prothrombin 20210A

27

acquired thrombophillia

antiphospholipid syndrome

28

clinical features of thrombophillaas

DVT, PE, superficial thrombophlebitis, thrombosis of the cerebral axillary, portal mesenteric veins, arterial thrombosis- unusual to be inherited.
arterial thrombosis- anti phospholipid syndrome
Coumarin induced skin necrosis (Protein C deficiency).
Obstetric complications : fetal wastage (Anti Phospholipid Syndrome)- due to thrombosis in the placental circulation.

29

where is the point mutation in factor V leiden

mutation in factor V gene were activated protein C cleaves factor V.

30

does protein C circulate in a activates or inactive form

inactive

31

what complex activates factor
protein C

thrombin and thrombomodulin

32

where is the point mutation in Prothrombin 20210A

untranslated region of prothrombin gene
increases pro thrombin levels

33

what are common clinical manifestations of antiphospholipid syndrome

• Venous thrombosis or
• Arterial thrombosis or
• Recurrent fetal loss (>2)

34

what is antiphospholipid syndrome seen in connection with

connective tissue disorders.

35

pathogenesis of Antiphospholipid syndrome

immune system produces abnormal antibodies called antiphospholipid antibodies. These target proteins attached to fat molecules (phospholipids), which makes the blood more likely to clot

36

if several miscarriages which thrombophilla is tested for

antiphospholipid antibody