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PathY5 > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

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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?

Study These Flashcards
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?

Study These Flashcards
A

Yes - oral is good for long term use

23
Q

How does warfarin work?

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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?

Study These Flashcards
A

INR between 2-3

derived from PT

25
Which drug is safe in pregnancy?
Heparin NOT WARFARIN, have to stop by 6 weeks
26
What is the half life for LMWH, UFH, Warfarin and DOACs?
LMWH - 6 hours UFH - 1-2 hours Warfarin - 2-3 days DOAC - 8-10 hours
27
How do you reverse heparin, warfarin and DOACs?
Heparin - protamine Warfarin - factor concentrate/ vitamin K DOAC- Ab to dabigatran, Xa in development
28
Who's at increased risk of thrombosis?
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
What Thromboprophylaxis is used?
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
What is included in the patient part of the Risk Assessment for VTE?
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
What is included in the procedure part of the Risk Assessment for VTE?
Hip or knee replacement Hip fracture Other major orthopaedic surgery Surgery > 30mins Plaster cast immobilisation of lower limb
32
What is included in the patient part of the bleeding risk assessment?
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
What is included in the procedure part of the bleeding risk assessment?
Neuro, spinal or eye surgery Other with high bleeding risk Lumbar puncture/spinal/epidural in previous 4 hours
34
What is the treatment pathway for DVT/ PE?
Immediate anticoagulation > Start LMWH > Stop LMWH when INR >2 for 2 days OR > Start DOAC - continue for 3-6 months
35
Give an example of a LMWH treatment that may be given for immediate treatment of DVT/ PE
Tinzaparin 175u/kg + warfarin
36
When would you thrombolyse a DVT/ PE?
Life threatening PE or limb threatening DVT There is a risk of haemorrhoage (4%) but reduces post phlebitic syndrome
37
Does the risk of thrombosis if untreated outweigh the risk of bleeding if treated?
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
How long do you anticoagulate the patient after first VTE after a surgical precipitant?
No need for long term
39
How long do you anticoagulate the patient after first VTE that was idiopathic?
You should consider long term
40
How long do you anticoagulate the patient after first VTE after a minor precipitant such as COCP, flights or trauma?
Usually 3 months adequate | Longer duration may be dictated by presence of other thrombotic and haemorrhagic risk factors
41
What is heparan?
Makes chemokine gradient across vessel wall
42
What do PGI2 and NO do?
Vasodilation and reduced platelet aggregation
43
what is immunothrombosis?
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
Which two risk factors stack?
Oral contraceptive pill | Factor V leiden
45
Which has a higher risk of thrombosis: FV leiden or Antithrombin deficiency?
Antithrombin deficiency
46
Which are the Vit K dependent clotting factors?
2, 7, 9, 10
47
Which condition do we always use warfarin for thromboprophylaxis?
Prosthetic valves
48
Which has less intercranial bleeding risk, DOAC or warfarin?
DOACs
49
Men or women: who has a higher recurrence?
Men
50
What position thrombosis has a higher rate of recurrence?
Proximal (popliteal and above)
51
Which drug-drug interactions are important?
Lots, carbamazepine, rifampicin | antibiotics and anti epileptics etc.

PathY5 (98 decks)

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