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PathY5 > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

How many hospital deaths are caused by PE?

A

5-10% - 1 in 1000 - 10,000 pa

25,000 deaths pa from hospital related VTE

Incidence doubling each decade

PE’s are preventable but difficult to reverse

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2
Q

What are the consequences of thromboembolism (and how common are they?)

A

Death - 5% mortality

Recurrence- 20% in first 2 years and 4% pa after

Thrombophlebitic syndrome - Severe TPS in 23% at 2 years, 11% with stockings

Pulmonary hypertension - 4% at 2 years

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3
Q

What increases the risk of thrombosis?

A

Virchow’s triad:
- Blood - hypercoagulability

  • Vessel wall - Sticky and injured
  • Blood flow - stasis
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4
Q

What causes Blood to be more prone to coagulation?

A
  • Viscosity from haematocrit/ protein/ paraprotein
  • Platelet count high
  • Excess pro-coagulant activity
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5
Q

Recite the summarised clotting cascade

A

Tissue factor and factor 7a increase F9a and the conversion of F10 to F10a

F8a also converts F10 to F10a

F5 a converts prothrombin to thrombin (F2a) which converts fibrinogen to fibrin and increases clotting

Thrombin also has a positive feedback loo on F8 and F5

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6
Q

Which factors are pro coagulant?

A 
V
VIII 
XI 
IX
X
II
Fibrinogen
Platelets
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7
Q

What are the anticoagulants?

A

Tissue factor pathway inhibitor (TF and 7a inhibitor)

Protein C and S (10a and 5a inhibitor)

Antithrombin (5a and thrombin inhibitor)

Thrombomodulin

EPCR

Fibrinolysis

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8
Q

What happens to the balance of pro and anti coagulants in thrombophilia?

A

More procoagulants

Less anticoagulants

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9
Q

What happens over time in pts with genetic Thrombosis risk?

A

As age increases, the risk of thrombosis free survival decreases and this risk is increased in those with genetic defects of thrombosis

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10
Q

Is the vessel wall normally antithrombotic or prothrombotic and why?

A

Anti thrombotic:
1. Expresses anticoagulant molecules (thrombomodulin, Endothelial protein C receptor, TFPI, heparans)

  1. Does not express TF
  2. Secretes antiplatelets like prostacyclin and NO
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11
Q

What causes the vessel wall to become pro thrombotic?

A

Injury or inflammation:

  • Infection
  • Malignancy- risk increases with time spent after diagnosis
  • Vasculitis
  • Trauma
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12
Q

What happens when the vessel wall is in it’s prothrombotic state?

A

Anticoagulant molecules (eg TM) are down regulated

Adhesion molecules upregulated

TF may be expressed

Prostacyclin production decreased

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13
Q

How does stasis promote thrombosis?

A

Accumulation of activated factors

Promotes platelet adhesion

Promotes leukocyte adhesion and transmigration

Hypoxia produces inflammatory effect on endothelium

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14
Q

What are the causes of stasis?

A
  1. Immobility- surgery, travel (esp. >12hrs, 4.77 per million), paraparesis
  2. Compression- tumour, pregnancy
  3. Viscosity- polycythaemia, paraprotein
  4. Congenital- vascular abnormalities
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15
Q

A 23 year old woman comes in with a painful leg after a 16 hour flight, a doppler reveals a DVT, what medication could you consider giving them?

A

Immediate:

  • Heparin: unfractionated, LMWH
  • DOAC

Delayed:
- Vitamin K antagonist (warfarin)

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16
Q 
Through which route are:
Unfractionated heparin
Low molecular weight heparin	
Pentasaccharide 
given?
A

Unfractionated heparin: IV infusion

LMWH: Sub cutaneous

Pentasaccharie: Sub cutaneous

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17
Q

How do these drugs work:
Unfractionated heparin
Low molecular weight heparin
Pentasaccharide ?

A

Potentiating antithrombin and providing immediate risk

But need to think about renal disease and long term risk of osteoporosis

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18
Q

Which type of heparin needs to be monitored?

A

Unfractionated heparin - it has more variable kinetics and dose-response

However in Renal Failure and extremes of weight LMWH should be monitored too

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19
Q

How do you monitor heparin?

A

Unfractionated: APTT or anti 5 a assay

LMWH: Anti 5a assay

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20
Q

What are the types of DOACs?

A

Anti 10a (-xabans) and Anti 2a (dabigatran)

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21
Q

What are the properties of a DOAC?

A

Oral, rapid acting with short half life

Peaks at 3-4 hours, does not require monitoring

Also useful in the long term

22
Q

Is warfarin Oral?

A

Yes - oral is good for long term use

23
Q

How does warfarin work?

A

Indirectly- prevents recycling of Vit K so takes longer to work

F2/7/9 and 10 fall but so does Protein C & S (which are also Vit K dependent)

24
Q

How do we monitor warfarin?

A

INR between 2-3

derived from PT

25
Q

Which drug is safe in pregnancy?

A

Heparin

NOT WARFARIN, have to stop by 6 weeks

26
Q

What is the half life for LMWH, UFH, Warfarin and DOACs?

A

LMWH - 6 hours
UFH - 1-2 hours
Warfarin - 2-3 days
DOAC - 8-10 hours

27
Q

How do you reverse heparin, warfarin and DOACs?

A

Heparin - protamine
Warfarin - factor concentrate/ vitamin K
DOAC- Ab to dabigatran, Xa in development

28
Q

Who’s at increased risk of thrombosis?

A

Medical in patients
»Infection/inflammation, immobility (inc stroke), age

Patients with cancer
»Procoag molecules, inflammation, flow obstruction

Surgical patients
»Immobility, trauma, inflammation

Previous VTE, Family history, genetic traits

Obese

Elderly

29
Q

What Thromboprophylaxis is used?

A

Assess ALL patients on admission

LMWH - Tinzaparin 4500u /clexane 40mg OD
- does not require monitoring

TED stockings (surgery or heparin CI)

Flotron (intermittent pneumatic compression to reduce pressure)

Sometimes DOAC +/- aspirin (orthopaedics)

30
Q

What is included in the patient part of the Risk Assessment for VTE?

A

Age > 60yrs

Previous VTE

Active cancer

Acute or chronic lung disease

Chronic heart failure

Lower limb paralysis (excluding acute CVA)

Acute infection

BMI>30

31
Q

What is included in the procedure part of the Risk Assessment for VTE?

A

Hip or knee replacement

Hip fracture

Other major orthopaedic surgery

Surgery > 30mins

Plaster cast immobilisation of lower limb

32
Q

What is included in the patient part of the bleeding risk assessment?

A

Bleeding diathesis (eg haemophilia, VWD)

Platelets < 100

Acute CVA in previous month (H’gge or thromb)

BP > 200 syst or 120 dias

Severe liver disease

Severe renal disease

Active bleeding

Anticoag or anti-platelet therapy

33
Q

What is included in the procedure part of the bleeding risk assessment?

A

Neuro, spinal or eye surgery

Other with high bleeding risk

Lumbar puncture/spinal/epidural in previous 4 hours

34
Q

What is the treatment pathway for DVT/ PE?

A

Immediate anticoagulation

> Start LMWH

> Stop LMWH when INR >2 for 2 days

OR

> Start DOAC

  • continue for 3-6 months
35
Q

Give an example of a LMWH treatment that may be given for immediate treatment of DVT/ PE

A

Tinzaparin 175u/kg + warfarin

36
Q

When would you thrombolyse a DVT/ PE?

A

Life threatening PE or limb threatening DVT

There is a risk of haemorrhoage (4%) but reduces post phlebitic syndrome

37
Q

Does the risk of thrombosis if untreated outweigh the risk of bleeding if treated?

A

Need to assess:

> Risk of recurrence
>Morbidity and mortality of recurrence

> Risk of therapy (bleeding)
>Morbidity and mortality of bleeding
>Variation of risks with different therapies

38
Q

How long do you anticoagulate the patient after first VTE after a surgical precipitant?

A

No need for long term

39
Q

How long do you anticoagulate the patient after first VTE that was idiopathic?

A

You should consider long term

40
Q

How long do you anticoagulate the patient after first VTE after a minor precipitant such as COCP, flights or trauma?

A

Usually 3 months adequate

Longer duration may be dictated by presence of other thrombotic and haemorrhagic risk factors

41
Q

What is heparan?

A

Makes chemokine gradient across vessel wall

42
Q

What do PGI2 and NO do?

A

Vasodilation and reduced platelet aggregation

43
Q

what is immunothrombosis?

A

Neutrophils undergo NETosis - neutrophil elastase etc. on top of inflamed endothelium

Inflammation is an important part of thrombosis by activating neutrophils and endothelial cells

44
Q

Which two risk factors stack?

A

Oral contraceptive pill

Factor V leiden

45
Q

Which has a higher risk of thrombosis: FV leiden or Antithrombin deficiency?

A

Antithrombin deficiency

46
Q

Which are the Vit K dependent clotting factors?

A

2, 7, 9, 10

47
Q

Which condition do we always use warfarin for thromboprophylaxis?

A

Prosthetic valves

48
Q

Which has less intercranial bleeding risk, DOAC or warfarin?

A

DOACs

49
Q

Men or women: who has a higher recurrence?

A

Men

50
Q

What position thrombosis has a higher rate of recurrence?

A

Proximal (popliteal and above)

51
Q

Which drug-drug interactions are important?

A

Lots, carbamazepine, rifampicin

antibiotics and anti epileptics etc.

PathY5 (98 decks)

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