Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

a path 3 > HAEM: Venous Thrombosis > Flashcards

HAEM: Venous Thrombosis Flashcards

1
Q

What % of hospital deaths does PE account for?

A

5-10%

25000 deaths per annum related to VTE, difficult to reverse but preventable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the recurrence rate of VTE?

A

20% within 2 years and 4% pa after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the death rate from VTE?

A

5% die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the occurence of pulmonary hypertension with VTE?

A

4% at 2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Virchow’s triad?

A
  • blood - hypercoagulability
  • vessel wall - damage
  • blood flow - stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What factors in blood increase risk of VTE?

A
  1. Viscosity
    • Haematocrit
    • Protein/paraprotein
  2. Platelet count
  3. Coagulation system - net excess of procoagulant activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List some procoagulant and anticoagulant factors.

A

Procoagulant - V, VIII, XI, IX, X, II, Fibrinogen, Platelets

Anticoagulant - TFPI, Protein C, Protein S, Thrombomodulin, EPCR, Antithrombin, Fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
A

Reduced protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is VTE preventable in thrombophilias?

A

In thrombophilias, VTE is precipitated in 50% of cases so these are still preventable e.g. Factor V leiden, Protein C/S deficiency, antithrombin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What factors in vessel wall increase risk of VTE?

A
  1. Expresses anticoagulant molecules
    • Thrombomodulin
    • Endothelial protein C receptor (ERCP) - helps protein C become activated
    • Tissue factor pathway inhibitor - FT usually kept outside the circulation
    • Heparans - co-factor for antithrombin
  2. Does not express tissue factor
  3. Secretes antiplatelet factors e.g. Prostacyclin, NO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does inflammation make the endothelium prothrombotic?

A

Inflammaton/injury makes the vessel wall prothormbotic e.g. infection, malignancy, vasculitis, trauma

Effects:

  1. Anticoagulant molecules (eg TM) are down regulated
  2. TF may be expressed
  3. Prostacyclin production decreased
  4. Adhesion molecules upregulated
  5. Von Willebrand factor release –> platelet and neutrophil capture –> neutrophil extracellular traps (NETS) form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the role of neutrophils in ‘immunothrombosis’.

A

How neutrophils contribute to thrombosis has been termed “immunothrombosis” highlighting that inflammation is an important drive for thrombosis.

Neutrophils - under stimuli release DNA forming neutrophil extracellular traps which…

  1. captures vWD,
  2. releases histones which activates platelets,
  3. provides a surface for contact activation of coagulant pathways (FXII –> XIIa)
  4. contains neutrophil elastase which can break down TFPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does blood flow/stasis increase risk of thrombosis?

A

Stasis –> thrombosis because..

  • Accumulation of activated factors
  • Promotes platelet adhesion
  • Promotes leukocyte adhesion and transmigration
  • Hypoxia produces inflammatory effect on endothelium - adhesion, release of VWF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the causes of blood stasis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does flight distance/time affect PE occurrence?

A

The longer the flight the higher the risk of PE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does taking the OC and having FVL increase risk of thrombosis compared to the general population?

A

RR of VTE with FVL + OC = x35

OC alone = ~x5

FVL alone = ~x7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which of the inherited thrombophilias has the highest risk of thrombosis?

A

Antithrombin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A

Antithrombin - decline in antithrombin curve was steepest for this out of all the thrombophilias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the difference between high and low dose anticoagulant regimens?

A
  • high - therapeutic (to treat active clot)
  • low - prophylactic
20
Q

What are the “immediate” and “delayed” anticoagulant drugs?

A

Immediate

  • Heparin - Unfractionated heparin OR Low molecular weight heparin
  • Direct acting anti-Xa and anti-IIa

Delayed

  • Vitamin K antagonists e.g. warfarin
21
Q

What factors does warfarin act on?

A

2, 7 , 9 , 10

22
Q

How do heparins act?

A

Increase activity of antithrombin

23
Q

What are the different types of heparin and their routes of administration ? Is the action of each monitored?

A
  • Unfractionated heparin = iv infusion, monitored
  • Low molecular weight heparin = sub cut, no monitoring
  • Pentasaccharide = sub cut, no monitoring
24
Q

What are the advantages and disadvantages of heparin?

A

Advantages

  • Immediate effect - can be used for treatment of thrombosis

Disadvantages

  • injections
  • risk of osteoporosis
  • variable renal dependence
25
Q

What are the main targets of DOACs? Give an example of each.

A

Direct acting anticoagulants:

  1. Anti-Xa - Rivaroxaban, apixaban, edoxaban
  2. Anti-IIa - Dabigatran
26
Q

What are the advantages of DOACs?

A

Advantages:

  • Oral administration
  • Immediate acting + good for long-term use –peak in approx. 3-4 hours (cf LMWH)
  • Short half-life
  • No monitoring
27
Q

What is the MOA of warfarin?

A
  • Indirect effect by preventing recycling of Vit
  • Levels of procoagulant factors II, VII, IX & X fall

BUT levels of anticoagulant protein C and protein S also fall

28
Q

Can warfarin be used for treatment of VTE?

A

No - onset of action is delayed

29
Q

How is warfarin monitored and what is this based on? Why can warfarin not be taken in pregnancy?

A

INR - this is derived from prothrombin time (PT)

Teratogenic in pregnancy

30
Q

Summarise the advantages and disadvantages of warfarin.

A

Advantages:

  • Orally administered

Disadvantages:

  • Delayed onset of action
  • Causes fall of some anticoagulant factors - protein C + S
  • May interact with dietary vit K
  • Variable absorption
  • Interaction with other drugs - due to protein binding and competition/induction of cytochromes
  • Teratogenic in pregnancy
31
Q

Comapre and contrast heparin, warfarin and DOACs in terms of:

  • administration
  • action
  • onset
  • monitoring
  • half-life effect
  • reversal
  • pregnancy
A
32
Q

What is a safe INR a abalance of?

A

Balance between thrombosis (low INR) and bleeding (high INR) must be achieved

33
Q

List some patient risk factors for VTE.

A
  1. Being a medical in patient - Infection/inflammation, immobility (inc stroke), age
  2. Being a surgical patient - immobility, trauma, inflammation
  3. Cancer - procoag molecules, inflammation, flow obstruction
  4. Previous VTE, FH, genetic traits
  5. Obese
  6. Elderly
34
Q

Which hospital patients should be assessed for risk of VTE and how should they be managed?

A

“All admissions to hospital should be assessed for thrombotic risk and unless contraindication exists, receive heparin prophylaxis” - NICE

This is done with a standard risk assessment form which assesses for risk of VTE on one side, and risk of bleeding on the other.

35
Q

What are the types of thromboprophylaxis?

A
  • Low molecular weight heparin (LMWH) e.g: Tinzaparin 4500u/ Enoxaparin 40mg od, not monitored
  • TED Stockings (for surgery or if heparin contraindicated)
  • Intermittent pneumatic compression (increases flow)
  • Sometimes DOAC +/- aspirin (orthopaedics)
36
Q

What does a risk assessment for VTE entail?

A

Looks at patient and procedural factors which may increase risk of VTE.

Patient factors:

  • Age > 60yrs
  • Previous VTE
  • Active cancer
  • Acute or chronic lung disease
  • Chronic heart failure
  • Lower limb paralysis (excluding acute CVA)
  • Acute infection
  • BMI>30

Procedural factors:

  • Hip or knee replacement
  • Hip fracture
  • Other major orthopaedic surgery
  • Surgery > 30mins
  • Plaster cast immobilisation of lower limb
37
Q

What does a risk assessment for bleeding entail?

A

Looks at patient and procedural factors which may increase risk of bleeding.

Patient factors:

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

Procedural factors:

  • Neuro, spinal or eye surgery
  • Other surgery with high bleeding risk
  • Lumbar puncture/spinal/epidural in previous 4 hours
38
Q

Do proximal or distal VTEs have higher rates of recurrence?

A

Proximal e.g. above knee, have higher rates of recurrence

39
Q

What type of bleeding do DOACs reduce compared to warfarin?

A

Intracranial most reduced - this is generally what kills patients on warfarin

Need to balance the risk of bleeding with the risk of recurrence of thrombosis when assessing need for long term therapy.

40
Q

Do males or females have higher recurrence rates of thrombosis?

A

Males - unknown reasons so they require long term anticoagulation in some cases

41
Q
A

Man after a walk - 5 - he had no preventable risk

42
Q
A

LMWH therapeutic dose

NB: aspirin may work quite quickly but it is not a good anticoagulant for thrombosis.

43
Q
A

Abdo-pelvis CT

44
Q

What is the risk of recurrence of VTE in these scenarios?

  • Surgery
  • Idiopathic
  • COCP, flight, trauma
A

Very low after surgical precipitant - no need for long term anticoagulation

High after idiopathic VTE - consider long term anticoagulation – esp with DOAC

After minor precipitants (COCP, flights, trauma) - usually 3 months adequate; longer duration may be dictated by presence of other thrombotic and haemorrhagic risk factors

45
Q

What is the risk of recurrence in 2years in idiopathic VTE?

A

10-20% in 2yrs = risk of recurrence in idiopathic VTE

a path 3 (89 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions