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Flashcards in 44 Thrombosis risk factors Deck (27)
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1
Q

What are the causes of arterial thrombosis? (4).

A

Atherosclerosis.
Rupture of a atheromatous plaque.
Endothelial injury.
Platelet aggregation.

2
Q

What are the risk factors for arterial thrombi? (9).

A
Smoking.
Hypertension.
Hypercholesterolaemia.
Diabetes.
Family history.
Obesity.
Inactivity.
Age.
Male.
3
Q

Wat is the pathogenesis of venous thrombi? (2).

A

Venous stasis.

Hyper coagulable state.

4
Q

What are venous thrombi predominantly composed of?

A

Fibrin.

5
Q

What percentage of VTE are clinically silent?

A

80%

6
Q

What is post thrombotic syndrome?

A

Chronic leg symptoms after VTE damage.

Ulceration, redness, swelling.

7
Q

What proportion of VTE’s are hospital acquired?

A

2/3rds.

8
Q

What are the prophylactic strategies for VTE prevention?

A

Risk assessment on admission and repeat in 24 hours.

Small doses of blood thinners and compression stockings.

9
Q

What are the pharmacological methods of VTE prevention (5).

A
LMWH.
Fondaparinux.
Rivaroxaban.
Apixaban.
Dabigatran.
10
Q

What are the exclusion tests for VTE? (2).

A

Wells score.

D-dimers.

11
Q

What are D-dimers?

A

Cross-linked molecules produced when plasmin breaks down fibrin clots. Specific to fibrin break down.

12
Q

What are D-Dimers good at in VTE?

A

Good -ve predictive value.

13
Q

How are VTEs diagnosed?

A

D-dimer.
Ultrasound for DVT, CT scan for PE.
Possible VQ scan for PE.

14
Q

How is LMWH used in initiating VTE prevention?

A

Treat for at least five days AND overlap with warfarin until INR >2 for at least two consecutive days.

15
Q

Which novel anticoagulants have anti IIa mechanism?

A

Argatroban.

Bivalirudin.

16
Q

Contrast dose response for warfarin and new oral anticoagulants:

A

Warfarin: high dose variability.
NOACs: usually uniform.

17
Q

Define thrombophilia:

A

Familial or acquired disorder of heamostasis likely to predispose to thrombosis.
AND co-segregation with clinical thrombosis in pedigree.

18
Q

Simply define thrombophilia:

A

Patients who develop VTE:

spontaneously, of disproportionate severity, recurrently, or at an early age.

19
Q

What are the heritable thrombophilias? (6).

A
Antithrombin deficiency.
Protein C deficiency.
Protein S deficiency.
Activated Protein C resistance/FV Leiden.
Dysfibrinogenaemia.
Prothrombin 20210A.
20
Q

Name an acquired thrombophilia:

A

Antiphospholipid syndrome.

21
Q

What does antithrombin inhibit?

A

Xa.

Ia (thrombin).

22
Q

How does thrombin act as an anti-coagulant?

A

Binds to thrombomodulin on endothelial surface. Thrombin-thrombomodulin complex activates protein C, which degrades FVa and FVIIIa.

23
Q

What is factor V Leiden?

A

Activated protein C resistance.

24
Q

What is the risk of thrombosis in Factor V Leiden?

A

3-5x for heterozygote.

30-50x fo homozygote.

25
Q

What is the genetic basis of Factor V Leiden?

A

G to A at 1691.

Arg replaced by Gln at 506 amino acid.

26
Q

What is change in prothrombin 20210A?
Effect?
Who?

A

Point mutation in 3’ untranslated region of prothrombin gene.
Increased prothrombin levels.
Rare in Africa + Asia.

27
Q

What is antiphospholipid syndrome?

A

Antiphospholipid antibodies on at least 2 occasions 8 weeks apart with:
Venous or material thrombosis, or >2 foetal losses.

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