Thrombosis and risk factors of thrombosis Flashcards

1
Q

what is virchows triad

A

blood flow, composition of blood and vascular endothelial.

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2
Q

what is the primary cause of a arterial thrombosis

A

atherosclerosis.

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3
Q

what is the pathogenesis of a arterial thrombosis

A

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

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4
Q

risk factors for arterial thrombi formation

A

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

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5
Q

what is the main component of a venous thrombus

A

fibrin

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6
Q

what is the pathogenesis of venous thrombosis

A

venous stasis

hypercoagubale states.

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7
Q

symptoms of DVT

A

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

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8
Q

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

A

Pulmonary embolism

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9
Q

symptoms of PE

A

chest pain, breathlessness and haemotypysis.

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10
Q

how can hospital acquired VTE be prevented

A

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

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11
Q

how is hospital acquired VTE treated

A

care pathway- anticoagulant drugs.

If patient is at increased risk of bleeding provide stocking to improve circulation to the legs

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12
Q

what are the risk factors of VTE

A
  • 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
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13
Q

what molecules does unfractionated heparin work on.

A

anti thrombin (2 sites) and anti Xa

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14
Q

what molecule does LMW heparin bind

A

anti Xa, and anti thrombin

Factor Xa inhibitor

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15
Q

what molecule does Fondaparinux find to

A

anti Xa

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16
Q

what molecule do direct thrombin inhibitors act on

A

thrombin

17
Q

What does a d-dimer test show

A

D-dimer breakdown product form fibrin clot.

Indicates that a clot was previously present although it has now been broken down

18
Q

how can a ultrasound help diagnose a thrombus

A

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
Q

what is a spiral/multi sliced CT used for

A

detect PE

20
Q

what is a VQ scan

A

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

21
Q

treatment plan for a uncomplicated patient with dot

A

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

22
Q

which anticoagulants are used as both treatment and prevention of DVT

A
  • Rivaroxaban, Apixaban- direct factor Xa inhibitor
  • Dabigatran- diresct thrombin inhibitor.-oral.
  • Fondaparinux, LMWH- paraenteral
23
Q

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

A

3-6 months.

warfarin

24
Q

what are recurrent episodes Recurrent episodes of VTE.

A

Treat with long term anticoagulation.

Recurrent episodes of VTE.

25
Q

define thrombophillia

A

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

26
Q

common inherited thrombophillias

A
  • 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
Q

acquired thrombophillia

A

antiphospholipid syndrome

28
Q

clinical features of thrombophillaas

A

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
Q

where is the point mutation in factor V leiden

A

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

30
Q

does protein C circulate in a activates or inactive form

A

inactive

31
Q

what complex activates factor

protein C

A

thrombin and thrombomodulin

32
Q

where is the point mutation in Prothrombin 20210A

A

untranslated region of prothrombin gene

increases pro thrombin levels

33
Q

what are common clinical manifestations of antiphospholipid syndrome

A
  • Venous thrombosis or
  • Arterial thrombosis or
  • Recurrent fetal loss (>2)
34
Q

what is antiphospholipid syndrome seen in connection with

A

connective tissue disorders.

35
Q

pathogenesis of Antiphospholipid syndrome

A

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
Q

if several miscarriages which thrombophilla is tested for

A

antiphospholipid antibody